This document discusses alcohol poisoning and the effects of ethanol. It covers the categories of alcohols, ethanol uses including as a beverage and in medicine, toxicokinetics of ethanol absorption and metabolism, mechanisms of action on the body, acute and chronic poisoning symptoms, and treatment approaches for alcohol poisoning and chronic alcoholism.
Alcoholic ketoacidosis (AKA) is a metabolic complication that can occur in chronic alcohol abusers during periods of heavy drinking and malnutrition. It results from high levels of ketone bodies in the blood (ketosis) and low blood pH (acidosis). AKA develops when alcohol metabolism prevents the liver from producing glucose, forcing the body to break down fat and protein instead. This leads to ketone production and metabolic acidosis. Symptoms include vomiting, dehydration, and altered mental status. Treatment involves fluid resuscitation, electrolyte replacement, insulin administration, and treating any underlying infections. With prompt treatment, the prognosis for AKA is generally good.
Alcohol is metabolized through three main pathways: 1) cytosolic alcohol dehydrogenase and mitochondrial aldehyde dehydrogenase, 2) microsomal ethanol oxidizing system, and 3) non-enzymatic oxidation. Acetaldehyde produced during metabolism is toxic and can damage liver cells, potentially leading to alcoholic hepatitis or cirrhosis over time with heavy drinking. Genetic differences in alcohol and aldehyde metabolizing enzymes also influence toxicity. Moderate drinking may provide some benefits but heavy drinking overwhelms the liver's ability to metabolize alcohol safely.
This document summarizes key details about aminotransferases and alkaline phosphatase enzymes. It discusses how aminotransferases like aspartate aminotransferase (AST) and alanine aminotransferase (ALT) catalyze the transfer of amino groups between amino acids and ketoacids, and how their levels are measured to monitor liver damage. AST is more elevated in conditions like hepatitis while ALT is higher in viral hepatitis. Alkaline phosphatase requires magnesium as an activator and exists as isoenzymes in the liver, bone, placenta and intestine that can be differentiated through electrophoresis or immunochemical methods.
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.
The document discusses the Warburg effect, where cancer cells preferentially use glycolysis over oxidative phosphorylation to generate energy, even in the presence of oxygen. This allows cancer cells to rapidly proliferate by generating ATP and biomass through glycolysis. The effect occurs because cancer cells overexpress hypoxia-inducible factor 1, increasing glycolytic enzymes and decreasing mitochondrial function. While the exact cause is still unknown, the Warburg effect provides cancer cells a growth advantage and is exploited in PET scanning and as a target for potential anticancer drugs.
1. Alcohol poisoning can occur from both acute and chronic alcohol consumption and has effects throughout the body, especially the central nervous system, gastrointestinal tract, and liver.
2. Treatment for acute alcohol poisoning involves first aid measures like keeping the person awake and monitoring their symptoms, followed by further treatment in the hospital like gastric lavage and IV fluids.
3. Chronic alcohol use can lead to conditions like liver cirrhosis and Korsakoff's psychosis. Treatment focuses on medications to prevent further alcohol use and psychotherapy. Death from alcohol poisoning may result from related causes like traffic accidents, suicide, or organ failure.
This document discusses alcohol poisoning and the effects of ethanol. It covers the categories of alcohols, ethanol uses including as a beverage and in medicine, toxicokinetics of ethanol absorption and metabolism, mechanisms of action on the body, acute and chronic poisoning symptoms, and treatment approaches for alcohol poisoning and chronic alcoholism.
Alcoholic ketoacidosis (AKA) is a metabolic complication that can occur in chronic alcohol abusers during periods of heavy drinking and malnutrition. It results from high levels of ketone bodies in the blood (ketosis) and low blood pH (acidosis). AKA develops when alcohol metabolism prevents the liver from producing glucose, forcing the body to break down fat and protein instead. This leads to ketone production and metabolic acidosis. Symptoms include vomiting, dehydration, and altered mental status. Treatment involves fluid resuscitation, electrolyte replacement, insulin administration, and treating any underlying infections. With prompt treatment, the prognosis for AKA is generally good.
Alcohol is metabolized through three main pathways: 1) cytosolic alcohol dehydrogenase and mitochondrial aldehyde dehydrogenase, 2) microsomal ethanol oxidizing system, and 3) non-enzymatic oxidation. Acetaldehyde produced during metabolism is toxic and can damage liver cells, potentially leading to alcoholic hepatitis or cirrhosis over time with heavy drinking. Genetic differences in alcohol and aldehyde metabolizing enzymes also influence toxicity. Moderate drinking may provide some benefits but heavy drinking overwhelms the liver's ability to metabolize alcohol safely.
This document summarizes key details about aminotransferases and alkaline phosphatase enzymes. It discusses how aminotransferases like aspartate aminotransferase (AST) and alanine aminotransferase (ALT) catalyze the transfer of amino groups between amino acids and ketoacids, and how their levels are measured to monitor liver damage. AST is more elevated in conditions like hepatitis while ALT is higher in viral hepatitis. Alkaline phosphatase requires magnesium as an activator and exists as isoenzymes in the liver, bone, placenta and intestine that can be differentiated through electrophoresis or immunochemical methods.
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.
The document discusses the Warburg effect, where cancer cells preferentially use glycolysis over oxidative phosphorylation to generate energy, even in the presence of oxygen. This allows cancer cells to rapidly proliferate by generating ATP and biomass through glycolysis. The effect occurs because cancer cells overexpress hypoxia-inducible factor 1, increasing glycolytic enzymes and decreasing mitochondrial function. While the exact cause is still unknown, the Warburg effect provides cancer cells a growth advantage and is exploited in PET scanning and as a target for potential anticancer drugs.
1. Alcohol poisoning can occur from both acute and chronic alcohol consumption and has effects throughout the body, especially the central nervous system, gastrointestinal tract, and liver.
2. Treatment for acute alcohol poisoning involves first aid measures like keeping the person awake and monitoring their symptoms, followed by further treatment in the hospital like gastric lavage and IV fluids.
3. Chronic alcohol use can lead to conditions like liver cirrhosis and Korsakoff's psychosis. Treatment focuses on medications to prevent further alcohol use and psychotherapy. Death from alcohol poisoning may result from related causes like traffic accidents, suicide, or organ failure.
This document discusses galactosemia, a rare genetic disorder that affects the body's ability to process galactose. Galactose is produced when lactose is broken down in the body. Normally it is converted to glucose for energy, but in galactosemia there is a deficiency in the enzyme galactose-1-phosphate uridyltransferase, preventing this process. As a result, galactose builds up in tissues and can cause issues like jaundice, cataracts, intellectual disability and liver/kidney problems. The disorder is treated by removing galactose and lactose from the diet. There are three types of galactosemia based on the specific enzyme deficiency.
The Warburg effect describes the observation that cancer cells rely heavily on glycolysis for energy production even when oxygen is plentiful. This differs from normal cells which primarily use oxidative phosphorylation. Otto Warburg first observed this phenomenon in the 1920s. The Warburg effect provides cancer cells with metabolic intermediates needed for rapid cell division and helps maintain a viable ATP/ADP ratio. It is driven by oncogene expression and hypoxia-inducible factors that increase glycolytic enzyme expression. While less efficient energetically, it allows cancer cells to proliferate quickly in changing tumor conditions. Understanding tumor cell metabolism provides opportunities for developing new anticancer therapies.
This document discusses lipid profile testing and the determination of various lipids in the blood, including total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, and others. It provides information on the clinical significance and normal ranges of each lipid, as well as methods for estimating and measuring the different lipids. Key points covered include the importance of cholesterol for various body functions but that too much can lead to health issues; sources of cholesterol from the body and diet; and the relationships between HDL, LDL, and risk for coronary artery disease.
This document discusses toxic alcohols including ethanol, methanol, ethylene glycol, and isopropanol. It provides details on the sources, metabolism, clinical effects, diagnosis, and treatment of toxic alcohol poisoning for each substance. Key points include the different metabolic pathways, symptoms based on serum concentration levels, use of antidotes like ethanol or fomepizole to prevent metabolism, and indications for hemodialysis in severe poisonings.
Buffer is a mixture of weak acid and salt of conjugate base that resist the change in pH upon the addition of acid or base.BUFFER + H+ H+ BUFFER.
TYPES OF BIOLOGICAL BUFFER1. Bicarbonate Buffer2. Phosphate Buffer3.Protein Buffer4. Haemoglobin
Liver function tests and interpretation is a very important topic for students of medical and allied fields. It is essential for efficient practice of clinical and laboratory medicine.
This document summarizes key aspects of metabolism integration. It discusses the major macronutrients and their roles in energy production and storage. The major metabolic pathways are described, including their junction points and regulatory enzymes. Specific pathways for glucose, fatty acids, and amino acids are explained. The roles of the liver in metabolic integration and regulation by hormones like insulin and glucagon are highlighted.
Cyclic AMP is a second messenger that mediates hormone signaling in cells. It is synthesized from ATP by adenylate cyclase in response to hormones like epinephrine and glucagon. Cyclic AMP activates protein kinase A, which causes effects like glycogenolysis, lipolysis, modulation of gene transcription, hormone secretion, increased gastric acid secretion, and regulation of cell permeability to water.
Prostaglandin, leukotriene, and thromboxaneGeeta Jaiswal
Eicosanoids are signaling molecules derived from polyunsaturated fatty acids like arachidonic acid. They are involved in complex control over inflammation, immunity, and the central nervous system. Eicosanoids are synthesized through the enzymatic oxidation of fatty acids by cyclooxygenase and lipoxygenase enzymes. They have short half-lives and act locally through autocrine and paracrine signaling. Examples of important eicosanoids include prostaglandins, thromboxanes, and leukotrienes.
1) Alcohol is absorbed in the stomach and intestine and metabolized primarily in the liver by alcohol dehydrogenase (ADH) and cytochrome P450 enzymes, converting it mainly to acetaldehyde and then acetate.
2) Some people have a mutated form of ADH that metabolizes alcohol more slowly, leading to more severe intoxication from smaller amounts of alcohol.
3) Chronic alcohol metabolism disrupts many metabolic pathways by altering the NADH/NAD+ ratio in the liver, which can cause issues like fatty liver, hypoglycemia, and lactic acidosis.
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.
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.
This document summarizes the structure and function of phospholipids and glycolipids. It describes that phospholipids are composed of a phosphate group attached to diacylglycerol or sphingosine, making them amphipathic. There are two main classes - phosphoglycerides which use glycerol as a backbone, and sphingomyelin which uses sphingosine. Phospholipids are synthesized in the endoplasmic reticulum and degraded by phospholipases. Glycolipids are composed of carbohydrates attached to ceramides via glycosidic bonds. They include neutral cerebrosides and acidic gangliosides and sulfatides.
Glycogen storage diseases are a group of inherited metabolic disorders caused by deficiencies of enzymes involved in glycogen breakdown or synthesis. This leads to abnormal glycogen buildup in tissues. The main types are GSD I, III and IV. In GSD I, glucose-6-phosphatase is deficient causing hypoglycemia and liver enlargement. GSD III results from a debranching enzyme defect causing abnormal glycogen structure. GSD IV involves branching enzyme deficiency and liver cirrhosis. Symptoms vary by type but may include low blood sugar, enlarged liver, muscle cramps and failure to thrive. Treatment focuses on a high-carbohydrate diet and cornstarch to manage blood sugar levels. Prognosis depends on
Slides prepared MBBS Biochemistry lectures. Includes description of hormone signaling, hormone actions, detailed description of insulin and diabetes mellitus, metabolic syndrome, thyroid hormones, calcium and phosphate homeostasis, vitamin D and PTH.
Prepared in Nov 2015
Alcohol is absorbed from the stomach and intestine and metabolized primarily in the liver. The liver enzyme alcohol dehydrogenase oxidizes ethanol to acetaldehyde, which is then further oxidized to acetate. A small amount of alcohol is eliminated through the lungs, urine, and sweat, while the majority is metabolized in the liver. The metabolism of alcohol increases the NADH/NAD+ ratio in the liver, leading to metabolic alterations like lactic acidosis, hypoglycemia, and fatty liver. Chronic alcohol use can also damage the liver and brain, potentially causing cirrhosis and neurological issues.
De novo fatty acid synthesis occurs in the liver, kidneys, and adipose tissue. It is a multi-step process that converts acetyl-CoA into palmitate using acetyl-CoA, ATP, NADPH, manganese, and biotin. The first step is transporting acetyl-CoA from the mitochondria to the cytosol. Fatty acid synthase, a large enzyme complex, then catalyzes the reactions that elongate the carbon chain by adding two carbon units from malonyl-CoA in each cycle until palmitate is produced. While most fatty acids come from diet, de novo synthesis provides lipids for certain tissues.
This document discusses glycogen metabolism pathways. It describes that glycogen metabolism has two pathways: glycogenesis and glycogenolysis. Glycogenesis is the formation of glycogen in the liver and muscles, requiring ATP and UTP. Glycogenolysis is the degradation of stored glycogen in the liver and muscles by glycogen degrading enzymes. Glycogen storage diseases can occur due to deficiencies in the enzymes involved in glycogenesis or glycogenolysis.
This document summarizes different classes of lipids, including eicosanoids, terpenoids, steroids, and phytosterols. It describes the structures and properties of prostaglandins, leukotrienes, lipoxins, terpenes, carotenoids, dolichol, coenzyme Q, cholesterol, bile acids, phytosterols like sitosterol and stigmasterol. Examples are provided of monoterpenes, sesquiterpenes, diterpenes, and tetraterpenes. The roles of these lipids in biological processes and potential applications are briefly mentioned.
The document discusses the reasons why people both choose to drink alcohol and choose to abstain. It then provides information on how alcohol passes through the body and is processed by the liver. Several factors that can influence how alcohol affects individuals are outlined, including body weight, food consumption, amount consumed, and expectations. Common effects of alcohol are listed, such as lowered inhibitions, impaired thinking and physical skills, diseases, tolerance, changes in body temperature, and hangovers. Treatment options for alcoholism are also briefly discussed.
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 galactosemia, a rare genetic disorder that affects the body's ability to process galactose. Galactose is produced when lactose is broken down in the body. Normally it is converted to glucose for energy, but in galactosemia there is a deficiency in the enzyme galactose-1-phosphate uridyltransferase, preventing this process. As a result, galactose builds up in tissues and can cause issues like jaundice, cataracts, intellectual disability and liver/kidney problems. The disorder is treated by removing galactose and lactose from the diet. There are three types of galactosemia based on the specific enzyme deficiency.
The Warburg effect describes the observation that cancer cells rely heavily on glycolysis for energy production even when oxygen is plentiful. This differs from normal cells which primarily use oxidative phosphorylation. Otto Warburg first observed this phenomenon in the 1920s. The Warburg effect provides cancer cells with metabolic intermediates needed for rapid cell division and helps maintain a viable ATP/ADP ratio. It is driven by oncogene expression and hypoxia-inducible factors that increase glycolytic enzyme expression. While less efficient energetically, it allows cancer cells to proliferate quickly in changing tumor conditions. Understanding tumor cell metabolism provides opportunities for developing new anticancer therapies.
This document discusses lipid profile testing and the determination of various lipids in the blood, including total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, and others. It provides information on the clinical significance and normal ranges of each lipid, as well as methods for estimating and measuring the different lipids. Key points covered include the importance of cholesterol for various body functions but that too much can lead to health issues; sources of cholesterol from the body and diet; and the relationships between HDL, LDL, and risk for coronary artery disease.
This document discusses toxic alcohols including ethanol, methanol, ethylene glycol, and isopropanol. It provides details on the sources, metabolism, clinical effects, diagnosis, and treatment of toxic alcohol poisoning for each substance. Key points include the different metabolic pathways, symptoms based on serum concentration levels, use of antidotes like ethanol or fomepizole to prevent metabolism, and indications for hemodialysis in severe poisonings.
Buffer is a mixture of weak acid and salt of conjugate base that resist the change in pH upon the addition of acid or base.BUFFER + H+ H+ BUFFER.
TYPES OF BIOLOGICAL BUFFER1. Bicarbonate Buffer2. Phosphate Buffer3.Protein Buffer4. Haemoglobin
Liver function tests and interpretation is a very important topic for students of medical and allied fields. It is essential for efficient practice of clinical and laboratory medicine.
This document summarizes key aspects of metabolism integration. It discusses the major macronutrients and their roles in energy production and storage. The major metabolic pathways are described, including their junction points and regulatory enzymes. Specific pathways for glucose, fatty acids, and amino acids are explained. The roles of the liver in metabolic integration and regulation by hormones like insulin and glucagon are highlighted.
Cyclic AMP is a second messenger that mediates hormone signaling in cells. It is synthesized from ATP by adenylate cyclase in response to hormones like epinephrine and glucagon. Cyclic AMP activates protein kinase A, which causes effects like glycogenolysis, lipolysis, modulation of gene transcription, hormone secretion, increased gastric acid secretion, and regulation of cell permeability to water.
Prostaglandin, leukotriene, and thromboxaneGeeta Jaiswal
Eicosanoids are signaling molecules derived from polyunsaturated fatty acids like arachidonic acid. They are involved in complex control over inflammation, immunity, and the central nervous system. Eicosanoids are synthesized through the enzymatic oxidation of fatty acids by cyclooxygenase and lipoxygenase enzymes. They have short half-lives and act locally through autocrine and paracrine signaling. Examples of important eicosanoids include prostaglandins, thromboxanes, and leukotrienes.
1) Alcohol is absorbed in the stomach and intestine and metabolized primarily in the liver by alcohol dehydrogenase (ADH) and cytochrome P450 enzymes, converting it mainly to acetaldehyde and then acetate.
2) Some people have a mutated form of ADH that metabolizes alcohol more slowly, leading to more severe intoxication from smaller amounts of alcohol.
3) Chronic alcohol metabolism disrupts many metabolic pathways by altering the NADH/NAD+ ratio in the liver, which can cause issues like fatty liver, hypoglycemia, and lactic acidosis.
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.
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.
This document summarizes the structure and function of phospholipids and glycolipids. It describes that phospholipids are composed of a phosphate group attached to diacylglycerol or sphingosine, making them amphipathic. There are two main classes - phosphoglycerides which use glycerol as a backbone, and sphingomyelin which uses sphingosine. Phospholipids are synthesized in the endoplasmic reticulum and degraded by phospholipases. Glycolipids are composed of carbohydrates attached to ceramides via glycosidic bonds. They include neutral cerebrosides and acidic gangliosides and sulfatides.
Glycogen storage diseases are a group of inherited metabolic disorders caused by deficiencies of enzymes involved in glycogen breakdown or synthesis. This leads to abnormal glycogen buildup in tissues. The main types are GSD I, III and IV. In GSD I, glucose-6-phosphatase is deficient causing hypoglycemia and liver enlargement. GSD III results from a debranching enzyme defect causing abnormal glycogen structure. GSD IV involves branching enzyme deficiency and liver cirrhosis. Symptoms vary by type but may include low blood sugar, enlarged liver, muscle cramps and failure to thrive. Treatment focuses on a high-carbohydrate diet and cornstarch to manage blood sugar levels. Prognosis depends on
Slides prepared MBBS Biochemistry lectures. Includes description of hormone signaling, hormone actions, detailed description of insulin and diabetes mellitus, metabolic syndrome, thyroid hormones, calcium and phosphate homeostasis, vitamin D and PTH.
Prepared in Nov 2015
Alcohol is absorbed from the stomach and intestine and metabolized primarily in the liver. The liver enzyme alcohol dehydrogenase oxidizes ethanol to acetaldehyde, which is then further oxidized to acetate. A small amount of alcohol is eliminated through the lungs, urine, and sweat, while the majority is metabolized in the liver. The metabolism of alcohol increases the NADH/NAD+ ratio in the liver, leading to metabolic alterations like lactic acidosis, hypoglycemia, and fatty liver. Chronic alcohol use can also damage the liver and brain, potentially causing cirrhosis and neurological issues.
De novo fatty acid synthesis occurs in the liver, kidneys, and adipose tissue. It is a multi-step process that converts acetyl-CoA into palmitate using acetyl-CoA, ATP, NADPH, manganese, and biotin. The first step is transporting acetyl-CoA from the mitochondria to the cytosol. Fatty acid synthase, a large enzyme complex, then catalyzes the reactions that elongate the carbon chain by adding two carbon units from malonyl-CoA in each cycle until palmitate is produced. While most fatty acids come from diet, de novo synthesis provides lipids for certain tissues.
This document discusses glycogen metabolism pathways. It describes that glycogen metabolism has two pathways: glycogenesis and glycogenolysis. Glycogenesis is the formation of glycogen in the liver and muscles, requiring ATP and UTP. Glycogenolysis is the degradation of stored glycogen in the liver and muscles by glycogen degrading enzymes. Glycogen storage diseases can occur due to deficiencies in the enzymes involved in glycogenesis or glycogenolysis.
This document summarizes different classes of lipids, including eicosanoids, terpenoids, steroids, and phytosterols. It describes the structures and properties of prostaglandins, leukotrienes, lipoxins, terpenes, carotenoids, dolichol, coenzyme Q, cholesterol, bile acids, phytosterols like sitosterol and stigmasterol. Examples are provided of monoterpenes, sesquiterpenes, diterpenes, and tetraterpenes. The roles of these lipids in biological processes and potential applications are briefly mentioned.
The document discusses the reasons why people both choose to drink alcohol and choose to abstain. It then provides information on how alcohol passes through the body and is processed by the liver. Several factors that can influence how alcohol affects individuals are outlined, including body weight, food consumption, amount consumed, and expectations. Common effects of alcohol are listed, such as lowered inhibitions, impaired thinking and physical skills, diseases, tolerance, changes in body temperature, and hangovers. Treatment options for alcoholism are also briefly discussed.
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.
Alcohol affects many parts of the body. It initially causes an energizing effect but is actually a depressant that slows the central nervous system. As more alcohol is consumed, it impairs judgment, motor skills, and can lead to intoxication or even loss of consciousness. The liver works to break down alcohol but drinking too much overwhelms this system. Long term heavy use can damage the liver and brain. Fetal alcohol syndrome may also result if a pregnant woman drinks.
Alcohol addiction is a growing problem that can seriously impact health and relationships. Drinking is common at social events but can damage the body, such as the heart, liver, and brain, and cause issues like cancer or cirrhosis. Alcohol abuse puts people at risk for car accidents, domestic violence, and fetal alcohol syndrome, and children of alcoholics are more likely to experience abuse and neglect. While some drink to relax or have fun, it is important to understand the consequences of alcohol and make responsible choices.
The document discusses misconceptions about women and alcohol use. It notes that while research was initially focused on men, more recent decades of research have shown significant physiological, psychiatric, and social differences for women related to alcohol use. Women face unique risks such as a more rapid progression of alcohol use disorders and health consequences. Prevention and treatment need to address the stigma faced by women and be tailored to their specific needs.
This document discusses the effects of alcohol abuse. It begins by identifying reasons why people drink, such as social influence, peer pressure, and stress relief. It then describes some short-term effects of drinking too much like memory loss, sickness, and loss of control. Long-term effects are also outlined and include liver damage, heart disease, cancer, and alcohol dependency. The learning outcomes are to identify the effects of alcohol abuse and explain the short and long-term consequences.
This document discusses women's drinking habits and the risks of alcohol consumption. It notes that more women are drinking now than in the past. Women who are more likely to drink include those with a family history of drinking, a partner who drinks heavily, a history of depression or abuse, and an ability to "hold their liquor" better than others. The document also explains that women get drunker than men after drinking the same amount due to having less muscle, water, and a slower alcohol metabolism from hormones like estrogen. It provides tips for quitting drinking and recommendations that women have no more than one drink per day for health or three drinks per day for safety.
Alcohol consumption can have negative health and social effects, especially for teens. Alcohol is a depressant that slows brain activity and impairs coordination, perception, and judgment. Excessive drinking over time can lead to serious liver diseases like cirrhosis or hepatitis by overloading and damaging the liver cells. Teen drinking is common due to curiosity and social pressures, but it increases risks of accidents, injuries, and long-term health problems if drinking continues into adulthood.
Alcohol is the most popular psychoactive drug in Western societies. It is categorized as a depressant that is absorbed through the stomach and small intestine and distributed via bloodstream. Alcohol is metabolized in the liver, though a small percentage is not broken down. Blood alcohol concentration depends on factors like weight, drinking rate, and genetics. Acute effects include impaired judgment and motor skills, while long-term heavy use can damage major organs and increase cancer risks. Treatment programs aim to address alcohol abuse and dependence.
This document discusses ethyl alcohol, its clinical uses, toxicity, and treatments for alcoholism. It notes that ethyl alcohol is used as an antiseptic, rubefacient, and appetite stimulant. Toxicity includes acute intoxication, withdrawal syndrome, and long-term complications involving multiple organ systems. Treatments discussed include disulfiram (an aldehyde dehydrogenase inhibitor), naltrexone (an opioid antagonist), and acamprosate for reducing relapse. Disulfiram causes an aversive reaction if alcohol is consumed after its administration, acting as a deterrent from drinking.
Sara Jo Nixon, Ph.D.-
Member, RiverMend Health Scientific Advisory Board for Addiction & Psychiatry. Professor and co-Vice Chair , Director, Neurocognitive Laboratory, Department of Psychiatry, University of Florida
Dr. Nixon addresses the RiverMend Health Scientific Advisory Board on alcohol and its effect in women and treatment techniques for those seeking help.
For more information visit: http://www.rivermendhealth.com/scientific-advisory-board-addiction.html
Ethyl alcohol is absorbed quickly in the small intestine and slowly in the stomach. It is widely distributed throughout the body, crossing the blood-brain barrier and placenta. Alcohol is primarily metabolized in the liver by alcohol dehydrogenase and aldehyde dehydrogenase into acetate. Alcohol metabolism follows zero-order kinetics and is excreted primarily through exhaled air, urine, and sweat. Alcohol can interact with many drugs, increasing their effects and toxicity through inhibition of drug-metabolizing enzymes. Drinking during pregnancy increases risks of fetal alcohol syndrome, miscarriage, stillbirth, and low birth weight. Guidelines recommend no more than 1-2 drinks per day for men and a lower limit for women, and avoiding drinking if taking interacting
This document outlines an alcohol awareness presentation given by Kathy Muller at the University of Houston orientation. The presentation defines key terms related to alcohol and drugs and discusses facts versus myths about alcohol. It explains that alcohol is a psychoactive depressant drug and outlines moderate versus abusive drinking. The presentation aims to increase understanding of alcohol and its effects on the body and behavior.
This document discusses alcohol pharmacology and the effects of alcohol on the body. It begins with defining key terms like pharmacology, alcohol, and fermentation. It then outlines the physical effects of alcohol at different blood alcohol concentration levels. Various sections summarize the metabolism of alcohol in the liver, short and long term central nervous system and other organ effects, and the development of alcohol dependence. Tables show the percentages of students at Longwood University who report alcohol use and the citations used are listed at the end.
The document summarizes alcohol metabolism by three pathways: alcohol dehydrogenase (ADH), microsomal ethanol oxidizing system (MEOS), and fatty acid ethyl ester synthase. ADH is the primary pathway and converts ethanol to toxic acetaldehyde and then acetic acid. MEOS involves cytochrome P450 and can produce free radicals. Both pathways impact blood sugar and oxygen levels. Methanol is converted by ADH to toxic formaldehyde and formic acid, causing acidosis. Ethylene glycol is converted to toxic glycolate and oxalate, causing acidosis and organ damage. Treatment focuses on removing the alcohols and metabolites and addressing acidosis.
case presentation on alcohol withdrawal syndromeRumana Hameed
This document presents a case of a 55-year-old male patient admitted for alcohol withdrawal syndrome. The patient has a history of chronic alcohol use and a shrunken left eye for 3 months. On examination, the patient has an enopthalus left eye and is incoherent. Lab tests show diffuse cerebral atrophy and pthysis bulbi of the left eye. The patient is assessed with alcohol withdrawal syndrome and left eye pthysis bulbi. The treatment plan includes thiamine, chlordiazepoxide, benfortiamine, antibiotics, pantoprazole, dextrose fluids, and multivitamins. Potential drug interactions and adverse effects of the medications are discussed. Lifestyle counseling addresses avoiding triggers
The document discusses various types of alcohols including methanol, ethanol, and ethylene glycol. It summarizes ethanol's pharmacokinetics such as rapid absorption in the stomach and metabolism primarily by alcohol dehydrogenase in the liver. Chronic alcohol use can lead to tolerance, dependence, and alcoholism with withdrawal symptoms. Treatment involves detoxification with benzodiazepines and supplementation to replace vitamin deficiencies.
This document discusses the history and types of alcohol. It traces the origins of alcohol production back to biblical times when Noah drank wine. It then outlines the production of beer, wine and spirits by various ancient civilizations. The document defines different types of alcohols such as ethyl alcohol and methanol. It also lists common uses of alcohol including in beverages, solvents, and disinfectants. Finally, it discusses social uses of alcohol and some negative consequences of excessive alcohol consumption.
Primary metabolism produces compounds essential for growth like pyruvate and ethanol. Secondary metabolism functions are often unknown and produces specialized compounds in few species, like antibiotics. Secondary metabolites are usually produced after growth stops, possibly due to stress, and have various industrial and medical uses. Many are derived from primary metabolites like amino acids or share biosynthetic pathways with them.
DIGESTIVE SYSTEM CLASS 2 physiology.pptxJacobKurian22
The document summarizes the physiology of the digestive system. It describes the small intestine, which has villi that increase its surface area. The small intestine completes chemical digestion, absorbs nutrients, and secretes hormones like CCK and secretin. It discusses the roles and secretions of the pancreas, liver, and gallbladder in digestion. The large intestine absorbs water and synthesizes some vitamins as bacteria ferment remaining carbohydrates. Digestion involves the cephalic, gastric, and intestinal phases and is regulated by neural and hormonal mechanisms.
Skeletal muscle relaxants can act peripherally or centrally. Peripherally acting drugs include neuromuscular blockers like non-depolarizing agents (tubocurarine, vecuronium) and depolarizing agents (succinylcholine). Centrally acting drugs include baclofen, diazepam, dantrolene and tizanidine which reduce muscle tone by various mechanisms of action in the spinal cord or brain. The document discusses the classification, mechanisms of action, pharmacokinetics, drug interactions and adverse effects of various skeletal muscle relaxants.
The urea cycle disorders result from genetic mutations causing defects in the metabolism of extra nitrogen from protein breakdown. There are six enzymes in the urea cycle that convert ammonia into urea for excretion. Deficiencies in the first three enzymes (CPS1, OTC, ASS) or the cofactor NAGS cause severe hyperammonemia in newborns. Symptoms include irritability, lethargy, coma, hypothermia, and seizures. Treatment involves removing protein, giving nitrogen-scavenging drugs like sodium benzoate and sodium phenylacetate, arginine supplementation, and supportive care. Long-term management includes a low-protein diet and monitoring for complications.
Fluid and electrolyte balance in oral surgeryPunam Nagargoje
• ELECTROLYTE BALANCE
• Def: - concentration of individual electrolytes in the body fluid compartments is normal and remains relatively constant.
• Electrolytes are dissolved in body fluids
• Sodium predominant extracellular cation, and chloride is predominant extracellular anion. Bicarbonate also in extracellular spaces
• Electrolyte balance
• Na + (Sodium)
– 90 % of total ECF cations
– 136 -145 mEq / L
– Pairs with Cl- , HCO3- to neutralize charge
– Low in ICF
– Most important ion in regulating water balance
– Important in nerve and muscle function
• Electrolyte imbalances: Sodium
• Hypernatremia (high levels of sodium)
– Plasma Na+ > 145 mEq / L
– Due to ↑ Na + or ↓ water
– Water moves from ICF → ECF
– Cells dehydrate
• HYPERATREMIA
• Hypernatremia Due to:
– Hypertonic IV soln.
– Oversecretion of aldosterone
– Loss of pure water
• Long term sweating with chronic fever
• Respiratory infection → water vapor loss
• Diabetes – polyuria
– Insufficient intake of water .
• Clinical manifestations
of Hypernatremia
• Thirst
• Lethargy
• Neurological dysfunction due to dehydration of brain cells
• Decreased vascular volume
• TREATMENT OF HYPERNATREMIA:
• Lower serum Na+
– Isotonic salt-free IV fluid [5% dextrose]
– Oral solutions preferable
• Hyponatremia
• Overall decrease in Na+ in ECF
• Two types: depletional and dilutional
• Depletional Hyponatremia
Na+ loss:
– diuretics, chronic vomiting
– Chronic diarrhea
– Decreased aldosterone
– Decreased Na+ intake
• Clinical manifestations of Hyponatremia
• Neurological symptoms
– Lethargy, headache, confusion, apprehension, depressed reflexes, seizures and coma
• Muscle symptoms
– Cramps, weakness, fatigue
• Gastrointestinal symptoms
– Nausea, vomiting, abdominal cramps, and diarrhea
• Tx – limit water intake or
• discontinue medicines such as diuretics
• TREATMENT OF HYPONATREMIA
• Hyponatremia which develops quickly should be treated quickly & vice-versa
• Patients with severe hypoNa (<115) are at risk of neurological damage
• Too rapid correction causes CENTRAL PONTINE MYELINOLYSIS.
• Targeted rate of correction: 0.5-1.0 mEq/L/hour
• Raise plasma Na by <10-12 mEq/L on first day
• Correction @ rate >25mEq/L places at high risk for central pontine myelinolysis
• Hypokalemia
• Normal serum k+ conc is 3.5 to 5.0 mEq/l
• Serum K+ < 3.5 mEq /L
• Beware if diabetic
– Insulin gets K+ into cell
– Ketoacidosis – H+ replaces K+, which is lost in urine
• β – adrenergic drugs or epinephrine
• Causes of Hypokalemia
• Decreased intake of K+
• Increased K+ loss
– Chronic diuretics
– Acid/base imbalance
– Trauma and stress
– Increased aldosterone
– Redistribution between ICF and ECF
• Treatment of hypokalamia
• Metabolic acidosis increases serum K+ levels & vice versa
• Post-op patients on fluid therapy should receive approx 60mEq/day to prevent hypokalemia
• 1mEq/L fall in serum K+= 200-400 mEq total body K+ deficit
• Failure to ↑ Sr. K+ even after sufficient correction should
This document summarizes the pathophysiology and management of Cushing's syndrome. It discusses the etiology, clinical manifestations, diagnosis, and treatment of the condition. Cushing's syndrome is caused by prolonged exposure to excess glucocorticoids and can be ACTH-dependent or independent. The signs and symptoms involve changes in body composition, skin, bone, muscle, cardiovascular, metabolic and immune systems. Diagnosis involves biochemical tests and imaging. Treatment focuses on surgical resection of the underlying tumor or adrenal disease when possible to normalize cortisol levels and alleviate symptoms.
This document summarizes potassium disorders including hypokalemia and hyperkalemia. It discusses the normal physiology of potassium regulation and mechanisms that can lead to imbalances. For hypokalemia, causes include decreased intake, redistribution into cells, and increased loss from the kidneys or gastrointestinal tract. Hyperkalemia can result from shifts of potassium into the extracellular space, inadequate renal excretion, and excessive potassium intake. Clinical features and treatment approaches focusing on antagonizing cardiac effects, redistributing potassium into cells, and removing excess potassium are outlined.
This document provides an overview of fluids and electrolytes in surgical patients. It discusses body water volumes, osmotic pressure, signs and symptoms of volume disturbances, and various electrolyte abnormalities including hypernatremia, hyponatremia, hyperkalemia, and hypokalemia. Common causes and clinical manifestations of each electrolyte imbalance are presented. The document also reviews intravenous fluid types, including crystalloids like lactated Ringer's solution and normal saline, as well as colloid solutions. Fluid and electrolyte requirements in surgical patients are discussed. References utilized include Schwartz's Principles of Surgery and Sabiston Textbook of Surgery.
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.
FLUID AND ELECTROLYTE BALANCE AND IMBALANCE.pptxAnkita Gurav
This document provides an overview of fluid and electrolyte balance, including:
1) It defines key terms like osmolality, electrolytes, and classifications of body fluids and fluid compartments.
2) It describes common electrolyte imbalances like hyponatremia, hypernatremia, hypokalemia, and hyperkalemia and their causes and treatments.
3) It discusses fluid volume disturbances and conditions like edema, and summarizes signs and symptoms of volume deficits and excesses.
Cirrhosis is an end-stage liver disease characterized by fibrosis, regenerative nodules, and loss of liver architecture. Common causes include alcohol, hepatitis B/C, and non-alcoholic fatty liver disease. Cirrhosis can lead to portal hypertension, where increased resistance in the liver causes blood to back up in the portal vein. Complications of portal hypertension include variceal bleeding, ascites, and hepatic encephalopathy. Management involves treating the underlying cause, managing complications, and liver transplantation for severe disease.
This document summarizes acute inflammation. It describes that acute inflammation is rapid in onset, lasting minutes to days, and is characterized by edema and emigration of leukocytes. The major components of acute inflammation are alterations in vascular caliber and structural changes to blood vessels that allow emigration of leukocytes, which are then activated. Leukocytes migrate to the site of injury guided by chemotaxis and adhere to endothelial cells through cellular adhesion molecules before transmigrating into tissues to carry out phagocytosis and killing of microbes.
Inborn errors of metabolism revision notes TONY SCARIA
1. The document discusses various inborn errors of metabolism (IEM) including those affecting amino acid metabolism, organic aciduria, urea cycle disorders, and other conditions like alkaptonuria and albinism.
2. Common clinical features of IEM include vomiting, poor feeding, lethargy, seizures, and metabolic acidosis. Diagnosis involves newborn screening tests and characteristic laboratory findings in blood and urine.
3. Treatment depends on the specific IEM but may include dietary modifications such as protein restriction, supplementation with vitamins and cofactors, ammonia scavengers for urea cycle disorders, and dialysis in severe cases.
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired, life-threatening disease of the blood characterized by destruction of red Blood cells by the complement system, a part of the body's innate immune system.
The disease is characterized by destruction of red blood cells (hemolytic anemia), blood clots (thrombosis), and impaired bone marrow function (not making enough of the three blood components). It has been known to result from somatic mutations in the PIGA gene, which encodes phosphatidylinositol glycan class A (PIGA).Most treatments for PNH aim to reduce symptoms and prevent complications.
ENDOCRINE SYSTEM, by prof D C MikULEacKYChimaDaniel3
The endocrine system communicates through chemical messengers called hormones, working more slowly than the nervous system but over longer durations. The major endocrine glands include the hypothalamus and pituitary which regulate other glands, thyroid which regulates metabolism, adrenals which regulate stress response and metabolism, pancreas which regulates blood sugar, and reproductive organs. Hormones work through feedback loops to maintain homeostasis. Disorders can result from too much or too little hormone production or response. The endocrine system allows for coordinated regulation of growth, metabolism, and reproduction.
This document discusses sodium metabolism and disorders of sodium balance. It begins by outlining the normal functions of sodium in the body, including determining membrane potential and acid-base balance. It then describes normal sodium metabolism, handling, and regulation by factors like the kidneys, aldosterone, and antidiuretic hormone. The document also summarizes approaches to diagnosing and managing sodium imbalances like hyponatremia and hypernatremia. It stresses the importance of first assessing a patient's volume status and correcting deficits or excesses slowly to avoid complications in conditions like cerebral edema or encephalopathy.
Chronic renal failure is the progressive loss of kidney function over months or years. It is defined as a decline in glomerular filtration rate below 70-75% and is generally irreversible. It progresses through stages and is caused by conditions like diabetes, hypertension, and glomerulonephritis. Symptoms result from kidney's inability to regulate fluids, electrolytes, and waste and include edema, shortness of breath, fatigue, and neurological changes. Treatment focuses on slowing progression through blood pressure control, cholesterol medications, treating anemia, and dialysis or transplant for end-stage disease.
This document discusses short bowel syndrome, which is caused by a shortage of the small intestine due to various conditions. It can lead to malabsorption, diarrhea, malnutrition, and electrolyte imbalances. The main causes are resection of over half of the small intestine or loss of mucosal function. Management involves controlling fluid loss, diarrhea, and providing nutritional support through total parenteral nutrition or enteral feeds. Surgical techniques and intestinal transplantation may also be used in severe cases. The condition progresses through acute, adaptation, and maintenance phases as the remaining intestine adapts to increase absorption over time.
My FLUID AND ELECTROLYTES for medical personnel.pptxGloria682723
This document provides an overview of fluid and electrolyte balance in the human body. It discusses the composition and regulation of body fluids, electrolytes including sodium, potassium, calcium and magnesium. Key points covered include the distribution of electrolytes between intravascular, interstitial and intracellular compartments; causes and clinical features of electrolyte imbalances like hyponatremia, hypernatremia, hypokalemia, hyperkalemia, hypocalcemia, hypercalcemia; and treatment approaches for correcting electrolyte abnormalities.
Similar to Alcohol and its types, the tests associated with it and the clinical conditions arising from it. (20)
DNA structure, the bonds involved and it seperationMohit Adhikary
DNA structure, and the bonds that stabilizes it. The structural components, units and the proteins involved. Types of DNA and its separation methods. Chargaffs rule and its application
The structure of the cell membrane, the phospholipid layer distinguished to the break down of protein and the lipid layer. Their structural components and the molecular basis of it.
Diabetes mellitus, its types and compicationsMohit Adhikary
This document discusses types and complications of diabetes mellitus. It begins with an outline that defines diabetes and classifies diabetes types and complications as acute or chronic. It then discusses the various types of diabetes in more detail, including type 1 diabetes pathogenesis and genetic and environmental risk factors. Type 2 diabetes risk factors and pathophysiology involving insulin resistance and secretion are covered. Other specific rare genetic types are defined. The document concludes by examining acute complications like diabetic ketoacidosis and chronic complications involving microvascular and macrovascular involvement, as well as theories around how hyperglycemia may lead to these complications. Glycemic control studies proving the benefits of control are also summarized.
Electrophoresis, the types of electrophoresis and samples usedMohit Adhikary
The different types of electrophoresis, and the different types of electrophoresis are explained here, along with the different samples that can be electrophoresed.
The slides show the gastric and pancreatic function test along with the significance of these tests and the conditions in which the values of which increase.
Blood glucose regulation, glucose homeostasis, factors regulating and under S...Mohit Adhikary
The slides explain about blood glucose regulation, glucose homeostasis, factors regulating and under Special Circumstances. Factors regulating Blood glucose level include the hormonal and non-hormonal.
Structure of protiens and the applied aspectsMohit Adhikary
The slides explain the structures of proteins, the bond stabilizing the structure of amino acids, the different types of protein structures, the applied aspects and the newer advances in the protein structure.
The four candles,child and the conversation amongst eachotherMohit Adhikary
Four candles representing Peace, Faith, Love, and Hope were slowly burning in an ambiance. Peace and Faith extinguished as they felt unnecessary in a world of anger and fighting. Love also went out as people forgot its importance. When a child entered and saw the unlit candles, crying out that they were meant to stay lit, Hope responded that it could re-light the others. The child used the candle of hope to relight Peace, Faith, and Love.
Transcription and the various stages of transcriptionMohit Adhikary
Transcription and its stages, the enzymes involved, the steps of transcription, the regulators of transcription, post translation modifications, formation of the types of RNA, applied concept
Amino acids are the units of proteins, and understanding its chemistry and the the properties assists in understanding the functions of proteins. This gives in an idea to why a certain protein behaves in a certain way.
Glycogen is the storage from of glucose. The metabolism of glycogen both as glycogenolysis, breakdown of glycogen, and glycogenesis, formation of glycogen along with their regulation is briefed in the slides.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
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Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
7. ALCOHOL
• SUPPLIES CALORIES
• DEVOID OF MINERALS, PROTEINS AND VITAMINS
• INTERFERES WITH VITAMIN ABSORPTION FROM INTESTINE
• DECREASES THEIR STORAGE IN THE LIVER
• MODEST EFFECT ON FOLATE, VIT B6, THIAMINE, NIACIN AND VIT A
14. ALCOHOL KETOACIDOSIS
• POOR DIET
• RECURRENT VOMITING
• MISDIAGNOSED AS DIABETIC KETOSIS
• INCREASE IN KETONES
• MILD INCREASE IN BLOOD GLUCOSE
• LARGE ANION GAP
• MILD TO MODERATE INCREASE IN SERUM LACTATE
• Β-HYDROXYBUTYRATE/LACTATE RATIO BETWEEN 2:1 AND 9:1 (NORMAL 1:1).
15. MEOS PATHWAY
• P450-DEPENDENT MICROSOMAL ETHANOL OXIDIZING SYSTEM
• INVOLVING NADPH AND O2
• INCREASES IN ACTIVITY IN CHRONIC ALCOHOLISM
• GENERATES ACETALDEHYDE AND SUBSEQUENTLY ACETATE
• WHILE OXIDIZING BIOSYNTHETIC REDUCING POWER, NADPH, TO NADP+.
• BECAUSE IT USES OXYGEN, THIS PATHWAY GENERATES FREE RADICALS THAT DAMAGE TISSUES.
• MOREOVER, BECAUSE THE SYSTEM CONSUMES NADPH, THE ANTIOXIDANT GLUTATHIONE CANNOT BE
REGENERATED EXACERBATING THE OXIDATIVE STRESS.
16. • BELOW 100 MG/DL (22 MMOL/L), THE MEOS SYSTEM, (HIGH KM FOR ALCOHOL), CONTRIBUTES LITTLE.
• WHEN LARGE AMOUNTS OF ETHANOL ARE CONSUMED, THE ADH SYSTEM BECOMES SATURATED OWING
TO DEPLETION OF NAD+.
• ABOVE 100 MG/DL, THERE IS INCREASED CONTRIBUTION FROM THE MEOS SYSTEM, WHICH DOES NOT RELY
UPON NAD+
• DURING CHRONIC ALCOHOL CONSUMPTION, MEOS ACTIVITY INCREASES.
• CHRONIC ALCOHOL CONSUMPTION RESULTS ALSO IN THE INCREASED CLEARANCE OF OTHER DRUGS
ELIMINATED BY THE MEOS SYSTEM.
17. • LIVER MITOCHONDRIA CAN CONVERT ACETATE INTO ACETYL COA IN A REACTION
REQUIRING ATP.
• ENZYME IS THE THIOKINASE THAT NORMALLY ACTIVATES SHORT-CHAIN FATTY ACIDS.
• HOWEVER, FURTHER PROCESSING OF THE ACETYL COA BY THE CITRIC ACID CYCLE IS
BLOCKED, BECAUSE NADH INHIBITS
• ISOCITRATE DEHYDROGENASE AND A-KETOGLUTARATE DEHYDROGENASE
18. CONSEQUENCES OF ACETYL COA
ACCUMULATION
• ↑KETONE BODIES FORMATION, EXACERBATING THE ACIDIC CONDITION ALREADY RESULTING FROM THE
HIGH LACTATE CONCENTRATION.
• THE PROCESSING OF THE ACETATE IN THE LIVER BECOMES INEFFICIENT, LEADING TO A BUILDUP OF
ACETALDEHYDE.
• THIS VERY REACTIVE COMPOUND FORMS COVALENT BONDS WITH MANY IMPORTANT FUNCTIONAL
GROUPS IN PROTEINS, IMPAIRING PROTEIN FUNCTION.
• IF ETHANOL IS CONSISTENTLY CONSUMED AT HIGH LEVELS, THE ACETALDEHYDE CAN SIGNIFICANTLY
DAMAGE THE LIVER, EVENTUALLY LEADING TO CELL DEATH
19. ↑NADH
• INHIBITS FATTY ACID OXIDATION
• ↑FATTY ACID SYNTHESIS
• INCREASED ESTERIFICATION OF FATTY ACIDS IN TRIACYLGLYCEROL
• INCREASED LIPOGENESIS
• ↑ CHOLESTEROL SYNTHESIS FROM ACETYL-COA,
• ↑ LIPID PEROXIDATION
• CITRIC ACID CYCLE IS BLOCKED
• INHIBITS ISOCITRATE DEHYDROGENASE AND A-KETOGLUTARATE DEHYDROGENASE
• HYPERLACTIC ACIDEMIA
• DECREASES EXCRETION
OF URIC ACID-GOUT
20.
21. ETHANOL
• CNS ACTIONS OF ETHANOL PRONOUNCED DURING ABSORPTIVE PHASE THAN
ELIMINATION PHASE- PHENOMINON OF ACUTE TOLERANCE
• SYNERGISTIC ACTION WITH CNS DEPRESSIVE DRUGS
• DEATHS OCCURRED
22. MECHANISM OF CNS DEPRESSION
• ENHANCEMENT OF MAJOR INHIBITORY
NEURONS
• IMPAIRMENT OF EXCITATORY NEURONS
• INHIBITORY NEURONAL SYSTEM-GABA
23. GABA binds to post
synaptic receptor
subtype GABAA
This complex opens
Inward flux
of Cl-
Membrane
hyper
polarization
Decreased
electrical response
24. GABA MEDIATED INHIBITORY RESPONSE ENHANCED BY
• ETHANOL
• BARBITURATES
• BENZODIAZEPINES
• MOST GENERAL ANAESTHETIC AGENTS
25. • CNS EXCITATORY RESPONSE MEDIATED BY GLUTAMATE
• ETHANOL INHIBITS THE EXCITATORY RESPONSE MEDIATED BY CA ION GATED
GLUTAMATE RECEPTOR SUBTYPE N-METHYL D ASPARTATE(NMDA)RECEPTOR
• ↑ THE ACTIVITY OF PHENYLETHANOLAMINE N METHYLTRANSFERASE
NOREPENEPHRINE EPENEPHRINE
PNMT
• EPINEPHRINE IN TURN ACTIVATES PRESYNAPTIC Α2 RECEPTORS WHICH INHIBITS RELEASE
OF NOREPINEPHRINE
27. DELIRIUM TREMENS
• INTENSE ACUTE WITHDRAWL
• DELIRIUM- MENTAL CONFUSION, AGITATION AND FLUCTUATING LEVELS OF
CONSCIOUSNESS
• TREMENS- ↑ PULSE, BP AND RESPIRATION
• CONCOMITANT MEDICAL DISORDERS
28.
29. EFFECTS OF ETHANOL ON ORGAN SYSTEMS
NERVOUS SYSTEM
• BLACKOUT, AN EPISODE OF TEMPORARY ANTEROGRADE AMNESIA
• DISTURBED SLEEP
• DISTURBING DREAMS
• SNORING
• EXACERBATES SLEEP APNOEA
• IMPAIRED JUDGEMENT AND COORDINATION
30. CHRONIC ALCOHOLISM
• PERIPHERAL NEUROPATHY
• CEREBELLAR DEGENERATION OR ATROPHY-PROGRESSIVE UNSTEADY STANCE AND GAIT OFTEN
ACCOMPANIED BY MILD NYSTAGMUS
WERNICKE’S (OPHTHALMOPARESIS, ATAXIA, AND ENCEPHALOPATHY)
KORSAKOFF ’S (RETROGRADE AND ANTEROGRADE AMNESIA)
• THIAMINE DEFICIENCY
• TRANSKETOLASE DEFICIENCY
31. PSYCHIATRIC PROBLEMS
• IMPULSIVITY AND DISINHIBITION
• PREEXISTING SCHIZOPHRENIA OR MANIC DEPRESSIVE DISEASE
• ANXIETY DISORDERS SUCH AS PANIC DISORDER.
• INTENSE SADNESS LASTING FOR DAYS TO WEEKS IN THE MIDST OF HEAVY DRINKING
• AUDITORY HALLUCINATIONS
32. GASTROINTESTINAL SYSTEM
ESOPHAGUS AND STOMACH
• EPIGASTRIC DISTRESS AND GASTROINTESTINAL BLEEDING
• MALLORY-WEISS LESION
PANCREAS AND LIVER
• ACUTE PANCREATITIS
• ALCOHOL-INDUCED HEPATITIS, PERIVENULAR SCLEROSIS, AND CIRRHOSIS
33. • (A) ABDOMINAL X RAY OF A PATIENT WITH ALCOHOLIC PANCREATITIS. NOTE
THE SPECKLED CALCIFICATION (I.E., CALCIUM DEPOSITS) WITHIN THE
PANCREAS (MARKED BY ARROWS).
• (B) ABDOMINAL X RAY FROM A SUBJECT WITHOUT PANCREATITIS.
34. CANCER
• BREAST CANCER
• ORAL AND ESOPHAGEAL CANCERS
• RECTAL CANCERS
HAEMATOPOETIC SYSTEM
• INCREASE IN (MCV)
• ACCOMPANIED BY FOLIC ACID DEFICIENCY-HYPERSEGMENTED NEUTROPHILS, RETICULOCYTOPENIA
• MILD THROMBOCYTOPENIA
• CHRONIC HEAVY DRINKING-DECREASED PRODUCTION OF WBCS
35. CARDIOVASCULAR SYSTEM
• MILD TO MODERATE HTN
• CORONARY ARTERY DISEASE
• CARDIOMYOPATHY
• UNEXPLAINED ARRHYTHMIAS TO HEART FAILURE
“HOLIDAY HEART.”
• ATRIAL OR VENTRICULAR ARRHYTHMIAS, ESPECIALLY PAROXYSMAL TACHYCARDIA, CAN ALSO OCCUR
AFTER A DRINKING BINGE IN INDIVIDUALS SHOWING NO OTHER EVIDENCE OF HEART
• OBSERVED TRANSIENTLY IN THE MAJORITY OF ALCOHOLICS ENTERING TREATMENT.
36. GENITOURINARY SYSTEM CHANGES AND SEXUAL
FUNCTIONING
MEN
• MODEST DOSES-INCREASE SEXUAL DRIVE
CHRONIC ALCOHOLISM-
• IRREVERSIBLE TESTICULAR ATROPHY
• SHRINKAGE OF THE SEMINIFEROUS TUBULES,
• DECREASES IN EJACULATE VOLUME,
• LOWER SPERM COUNT
37. WOMEN
• AMENORRHEA, A DECREASE IN OVARIAN SIZE,
• ABSENCE OF CORPORA LUTEA WITH ASSOCIATED INFERTILITY,
• INCREASED RISK OF SPONTANEOUS ABORTION.
38. BONE
• CHANGES IN CALCIUM METABOLISM
• LOWER BONE DENSITY
• DECREASED GROWTH IN THE EPIPHYSIS
• ↑RISK OF FRACTURES
• OSTEONECROSIS OF FEMORAL HEAD
39. OTHER EFFECTS
• ALCOHOLIC MYOPATHY
• ↑CORTISOL
• ↑ VASOPRESSIN AT RISING BLOOD ALCOHOL CONC
• ↓ VASOPRESSIN AT FALLING BLOOD ALCOHOL CONC
• MODEST ↓ IN T4
• MARKED ↓ IN T3
40. FETAL ALCOHOL SYNDROME
• HEAVY DRINKING DURING PREGNANCY
• PLACENTAL TRANSFER OF ETHANOL AND ACETYLDEHYDE
43. CHRONIC ALCOHOLISM
• ↑GGT
• CARBOHYDRATE DEFICIENT TRANSFERRIN
• ABNORMAL PITUITORY, ADRENOCORTICAL AND
MEDULLARY FUNCTION
• DESIALYLATION OF PROTEINS
• ↑MCV
44. METHANOL
• CONSTITUENT OF ANTIFREEZE AND WINDOW CLEANING FLUIDS AND CANNED FUEL
• INTENSIONAL CONSUMPTION-ETHANOL SUBSTITUTE
• ACCIDENTALLY-ILLEGAL WHISKY
• ACCIDENTAL –CHILDREN
• CNS EFFECTS LESS SEVERE
THAN ETHANOL
• LIVER ADH
45. FORMIC ACID
• SERIOUS ACIDOSIS
• OPTIC NEUROPATHY
• BLINDNESS
• DEATH
• FORMATE IS TOXIC BECAUSE IT INHIBITS MITOCHONDRIAL CYTOCHROME C OXIDASE, CAUSING THE
SYMPTOMS OF HYPOXIA AT THE CELLULAR LEVEL, AND ALSO CAUSING METABOLIC ACIDOSIS
• SERUM FORMATE CORRELATE WITH ACIDOSIS AND SEVERITY OF CNS AND OCULAR TOXICITY THAN DO
SERUM METHNOL CONC
• ETHANOL IS SOMETIMES DENATURED (ADULTERATED), AND THUS MADE UNDRINKABLE, BY THE ADDITION
OF METHANOL. THE RESULT IS KNOWN AS METHYLATED SPIRIT
46. TREATMENT OF METHANOL INTOXICATION
• ETHANOL
• FOMEPIZOLE TO INHIBIT METHANOL METABOLISM
• SODIUM BICARBONATE THERAPY FOR METABOLIC ACIDOSIS
• FOLATE-ENHANCE FOLATE MEDIATED METABOLISM OF FORMATE
• HAEMODIALYSIS- CLEARANCE OF METHANOL AND FORMATE
47. ANALYSIS
• HEAD SPACE GAS CHROMATOGRAPHY-METHOD OF CHOICE FOR METHANOL
ESTIMATION
• ENZYMATIC ASSAY
• BASED ON FORMATE DEHYDROGENASE
48. ISOPROPANOL
• 70% AQUEOUS SOLUTION- RUBBING ALCOHOL
• TWICE THE CNS DEPRESSANT ACTION AS ETHANOL
• NOT AS TOXIC AS METHANOL
• SHORT HALF LIFE-6HOURS
• RAPIDLY METABOLISED BY ADH TO ACETONE WHICH IS ELIMINATED MORE SLOWLY(T1/2 17 TO27 HRS)
• ALVEOLAR AIR AND URINE
• ACETONE CONC EXCEEDS ISOPROPANOL IN ELIMINATION PHASE
49. ISOPROPANOL
• ACETONE-CNS DEPRESSANT ACTIVITY SAME LIKE ETHANOL
• LONGER HALF LIFE-PROLONGS THE CNS EFFECTS
SEVERE INTOXICATION-
• COMA OR DEATH
• TREATMENT- HAEMODIALYSIS
• ETHANOL NOT INDICATED
51. BLOOD ALCOHOL
• SERUM, PLASMA OR WHOLE BLOOD
• SITE CLEANSED WITH ALCOHOL FREE DISINFECTANT LIKE BENZALKONIUM CHLORIDE
• SERUM: WHOLE BLOOD ETHANOL RATIO IS 1.14
• SPECIMENS WELL CAPPED
• BLOOD PROPERLY SEALED-14 DAYS AT ROOM TEMP
• 4 DEG WITH OR WITHOUT PRESERVATIVE
• LONGER STORAGE-SODIUM FLUORIDE PRESERVATIVE
• NON STERILE POST MORTEM SPECIMENS-SODIUM FLUORIDE
52. ESTIMATION
• ENZYMATIC ANALYSIS USING ALCOHOL DEHYDROGENASE
• ETHANOL TO ACETALDEHYDE
• AMOUNT OF NADH FORMED AT 340NM
• ADH RELATIVELY SPECIFIC TO ETHANOL
• INTERFERENCE 7% -ISOPROPANOL, 3 % METHANOL AND 4 % ETHYLENE GLYCOL
• SPECTROPHOTOMETERS OR AUTOMATED ANALYSERS
• SERUM COMMONLY
• URINE OR SALIVA
• WHOLE BLOOD-PRECIPITATION STEP- AVOID HAEMOGLOBIN INTERFERENCE
53. BREATH ALCOHOL
• POINT OF CARE
• PRINCIPLE-ALCOHOL IN CAPILLARY ALVEOLAR BLOOD RAPIDLY EQUILIBRATES WITH
ALVEOLAR AIR IN A RATIO 2100:1(BLOOD:BREATH)
• BREATH ALCOHOL G/210L=G/DL IN WHOLE BLOOD
• BLOOD:BREATH=2100:1
• WAITING PERIOD-15 MIN
• VERY RECENT DRINKING, ALCOHOL CONTAINING MOUTHWASH OR VOMITING ALCOHOL
RICH GASTRIC JUICE
54. BREATH ALCOHOL
• ACTIVE ALCOHOL ABSORPTION-30-120 MIN
• ARTERIAL BLOOD ALCOHOL>PERIPHERAL VENOUS BLOOD
• BREATH ALCOHOL>VENOUS BLOOD BECAUSE END EXPIRATORY AIR EQUILLIBRATES
WITH PULMONARY ARTERIAL BLOOD
55. US DEPARTMENT OF TRANSPORTATION
• BREATH ALCOHOL
• 0.02-0.04G/210L-NO DUTIES FOR 8HRS
• 0.04G/210L-SUSPENDED FROM DUTY UNTIL EVALUATION BY SUBSTANCE ABUSE
PROFESSIONALS
56. BREATH ALCOHOL MEASUREMENT
• INFRA RED ABSORPTION SPECTROMETRY(MOST COMMON)
• DICHROMATE SULFURIC ACID OXIDATION REDUCTION
• GC(FLAME IONIZATIONOR THERMAL CONDUCTIVITY DETECTION
• ELECTROCHEMICAL OXIDATION
• METAL OXIDE SEMICONDUCTOR SENSORS
57. SALIVA ALCOHOL
• EASY
• NONINVASIVE
• ETHANOL DISTRIBUTION BETWEEN BLOOD AND SALIVA BY PASSIVE DIFFUSION
• 9%HIGHER THAN WHOLE BLOOD
• SIMILAR TO SERUM ALCOHOL
• CONCENTRATION TIMES SAME IN BLOOD, BREATH AND SALIVA
58. QED SALIVA ALCOHOL TEST
• ETHANOL IN SALIVA
• ADH REACTION COUPLED WITH DIAPHORASE MEDIATED COLOUR INDICATOR REACTION
• RESULTS IN AGREEMENT WITH VENOUS BLOOD OR BLOOD
• ON SITE USE
• EMERGENCY DEPT, WORKPLACE, ROADSIDE
• APPROVED BY DOT FOR ALCOHOL SCREENING
• DESIGNED FOR SALIVA
• ACCURATE MEASUREMENT OF SERUM ETHANOL AS WELL
59. QED TEST
USING THE COTTON SWAB INCLUDED, ACTIVELY SWAB
AROUND THE CHEEKS, GUMS, AND TONGUE FOR 30-60
SECONDS OR UNTIL THE COTTON SWAB IS COMPLETELY
SATURATED WITH SALIVA
PLACE THE TEST DEVICE ON A FLAT SURFACE. GENTLY TWIST THE
SWAB WITH THE COLLECTED SALIVA SAMPLE INTO THE ENTRY PORT
AND APPLY STEADY PRESSURE TO ACTIVATE THE CAPILLARY ACTION
UNTIL THE PINK FLUID PASSES THE QA SPOT™ LOCATED AT THE
TOP OF THE TEST DEVICE.
READ THE TEST RESULTS. ALLOW THE TEST DEVICE TO DEVELOP FOR
TWO MINUTES. A DISTINCT PURPLE BAR WILL FORM WITHIN THE
MARKED SCALE REGION. THE HIGHEST POINT OF THE PURPLE BAR
REPRESENTS THE LEVEL OF ALCOHOL EXPRESSED AS EITHER A
PERCENTAGE (.0X%) OR MILLIGRAMS (ML/DL) CONCENTRATION.
60. • U.S. DEPARTMENT OF TRANSPORTATION (DOT)
• ALCOHOL TESTING FORM
• (THE INSTRUCTIONS FOR COMPLETING THIS FORM ARE ON THE BACK OF COPY 3)
• STEP 1: TO BE COMPLETED BY ALCOHOL TECHNICIAN
• A: EMPLOYEE NAME______________________________________________________________________________________
• (PRINT) (FIRST, M.I., LAST)
• B: SSN OR EMPLOYEE ID NO. _____________________________________________________________________________
• C: EMPLOYER NAME _____________________________________________________________________________
• STREET CITY, ST ZIP _____________________________________________________________________________
• DER NAME AND
• TELEPHONE NO. ___________________________________________________(_____)____________________
• DER NAME DER PHONE NUMBER
• D: REASON FOR TEST: . RANDOM . REASONABLE SUSP . POST-ACCIDENT .RETURN TO DUTY . FOLLOW-UP . PRE-EMPLOYMENT
• STEP 2: TO BE COMPLETED BY EMPLOYEE
• I CERTIFY THAT I AM ABOUT TO SUBMIT TO ALCOHOL TESTING REQUIRED BY US DEPARTMENT OF TRANSPORTATION REGULATIONS AND THAT THE
• IDENTIFYING INFORMATION PROVIDED ON THE FORM IS TRUE AND CORRECT.
• ___________________________________________________________________ _____________/____/_____
• SIGNATURE OF EMPLOYEE DATE MONTH DAY YEAR
• STEP 3: TO BE COMPLETED BY ALCOHOL TECHNICIAN
• (IF THE TECHNICIAN CONDUCTING THE SCREENING TEST IS NOT THE SAME TECHNICIAN WHO WILL BE CONDUCTING THE CONFIRMATION TEST,
• EACH TECHNICIAN MUST COMPLETE THEIR OWN FORM.) I CERTIFY THAT I HAVE CONDUCTED ALCOHOL TESTING ON THE ABOVE NAMED
• INDIVIDUAL IN ACCORDANCE WITH THE PROCEDURES ESTABLISHED IN THE US DEPARTMENT OF TRANSPORTATION REGULATION, 49 CFR PART
61. • TEST # TESTING DEVICE NAME DEVICE SERIAL # OR LOT # & EXP DATE ACTIVATION TIME READING TIME RESULT
• CONFIRMATION TEST: RESULTS MUST BE AFFIXED TO EACH COPY OF THIS FORM OR PRINTED DIRECTLY ONTO THE
FORM.
• REMARKS:
• __________________________________________________________________________________________
• ALCOHOL TECHNICIAN’S COMPANY COMPANY STREET ADDRESS
• _______________________________________________
_______________________________(_____)_________________
• (PRINT) ALCOHOL TECHNICIAN’S NAME (FIRST, M.I., LAST) COMPANY CITY, STATE, ZIP PHONE NUMBER
• _______________________________________________ __________/____/________
• SIGNATURE OF ALCOHOL TECHNICIAN DATE MONTH DAY YEAR
• STEP 4: TO BE COMPLETED BY EMPLOYEE IF TEST RESULT IS 0.02 OR HIGHER
• I CERTIFY THAT I HAVE SUBMITTED TO THE ALCOHOL TEST, THE RESULTS OF WHICH ARE ACCURATELY RECORDED ON
THIS FORM. I UNDERSTAND
• THAT I MUST NOT DRIVE, PERFORM SAFETY-SENSITIVE DUTIES, OR OPERATE HEAVY EQUIPMENT BECAUSE THE
RESULTS ARE 0.02 OR GREATER.
• ______________________________________________________________________
_____________/_____/____
• SIGNATURE OF EMPLOYEE DATE MONTH DAY YEAR
• OMB NO. 2105-0529
62. ONSITE ALCOHOL TEST CARD DEVICE
• SALIVA OR URINE
• SAME REACTION
• POSITIVE RESPONSE FOR ETHANOL CONCENTRATION GREATER THAN 0.02G/DL
• ALSO APPROVED BY DOT
63. THIRD DEVICE
• PLASTIC TEST STRIP
• DOT APPROVED
• ADH DIAPHORASE COUPLED INDICATOR COLOUR BAR
• IF 0.02G/DL OR GREATER
64.
65. COLLECTION DIFFICULT
• FLOW OF SALIVA UNDER CONTROL OF PARASYMPATHETIC NERVOUS SYSTEM
• ANTICHOLINERGIC SYMPTOMS
• DRY MOUTH ASS WITH TCA OVERDOSE
• SALIVARY FLOW MAY BE IMPAIRED IN SOME ALCOHOLICS
66. URINE ALCOHOL
• ALTERNATIVE TO SALIVA
• LESS INVASIVE THAN BLOOD
• POST ABSORPTIVE PHASE-CONCENTRATION 1.3 TIMES BLOOD
• DISCOURAGED BY SOME AS THIS RATIO IS HIGHLY VARIABLE
• REPRESENTS AN AVERAGE OF BLOOD ALCOHOL
• EMPTYING THE BLADDER, COLLECTING URINE AFTER 20 TO 30 MIN
• PREVIOUS 8 HRS
• NOT APPROVED BY DOT
68. ALCOHOLIC LIVER DISEASE
RISK FACTORS
1.DURATION AND MAGNITUDE OF ETHANOL INGESTION
• THRESHOLD 40G/DAY IN MEN AND 10G/DAY IN WOMEN
• RISK DOSE-80G/DAY(200ML OF WHISKY OR EQUIVALENT)
• DAILY DRINKING RISKIER
69. 2. GENDER-WOMEN
• GREATER LIKELYHOOD OF PROGRESSION TO CIRRHOSIS
• WOMEN HAVE REDUCED ACTIVITIES OF ADH
3. HEPATITIS B OR C
• INCREASE THE SEVERITY IN PATIENTS WHO DRINK HEAVILY
4.GENETIC FACTORS
• INHERITED PREDISPOSITION TO ALCOHOLISM
70. 5. NUTRITIONAL STATUS
• PROTEIN CALORIE MALNUTRITION
• POOR INTAKE
• ABNORMAL NUTRIENT METABOLISM
• OBESITY MAY BE A RISK FACTOR
72. LIVER DAMAGE FROM EXCESSIVE ETHANOL CONSUMPTION OCCURS IN
THREE STAGES.
1. FATTY LIVER.
1. GOOD PROGNOSIS
2. STEATOSIS DISAPPEARS AFTER 3 MONTHS OF ABSTINANCE
2. ALCOHOLIC HEPATITIS
WORSE PROGNOSIS
3. CIRRHOSIS
• THE CIRRHOTIC LIVER IS UNABLE TO CONVERT AMMONIA INTO UREA,
• AMMONIA IS TOXIC TO THE NERVOUS SYSTEM AND CAN CAUSE COMA AND
DEATH.
73. ACUTE ALCOHOLIC HEPATITIS
• ACUTE FEBRILE ILLNESS
• LEUCOCYTOSIS
• ↑ACUTE PHASE PROTEINS
• AST>2 TIMES ALT
• CHOLESTATIC FORM WITH ↑ ALP>3 TIMES MAY BE SEEN-HIGHER MORTALITY
• ↑BILIRUBIN, ↓ALBUMIN AND PT-POOR PROGNOSIS
74. GENETIC COMPONENT
• BOTH ALCOHOLISM AND SUSCEPTIBILITY TO THE DEVELOPMENT OF CIRRHOSIS
• VARIATION IN ALCOHOL INTAKE-GENETIC
• GENETIC POLYMORPHISM OF THE (MEOS) MICROSOMAL ETHANOL OXIDISING SYSTEM AND ADH
• 50% ASIANS HAVE ABSENT ADH-FLUSH REACTION TO ALCOHOL THAT INHIBITS DRINKING
• HETEROZYGOTES OF ACETALDEHYDE DEHYDROGENASE(AADH)-IMPAIRED CLEARANCE OF
ACETALDEHYDE-PUTATIVE TOXIN-LIVER INJURY
75. FATTY LIVER
• ACCUMULATION OF FATTY ACIDS IN THE LIVER
• ENDOGENOUS SYNTHESIS
• NO IMPAIRMENT OF HEPATIC SYNTHESIS OF PROTEIN AFTER ETHANOL INGESTION
76.
77. FATTY LIVER
• ↑ACETYL COA- ↑ FATTY ACID SYNTHESIS
• ACETALDEHYDE-PRIMARY TOXIN
• CAUSES GENERATION OF FREE RADICALS
• DEPLETION OF ANTI-OXIDANTS, LIKE GLUTATHIONE
• INJURY TO LIVER CELLS
• INDUCTION OF COLLAGEN SYNTHESIS- FIBROSIS AND CIRRHOSIS
79. BIOCHEMICAL MARKERS
AMINO TRANSFERASES
• AMINO TRANSFERASE ACTIVITIES RARELY EXCEED 300U/L-ACUTE ALCOHOLIC
HEPATITIS
• MUCH LOWER IN CHRONIC LIVER DISEASE
• ALCOHOL DEPLETES THE VIT B6 DEPENDENT PYRIDOXAL 5 PHOSPHATE-PRECURSOR
OF AMINO TRANSFERASE
• AST:ALT>2
80. BIOCHEMICAL MARKERS
• ↑APPEARANCE OF MITOCHONDRIAL AST(MAST)
• NOT SOLE CAUSE
• DAMAGE TO OTHER TISSUES WHICH RELEASE AST BUT NOT ALT, CONFINED TO LIVER
ALP ELEVATED 2 TO 4 FOLD
GGT
• GGT-SCREENING TEST
• GGT-INDUCIBLE ENZYME ELEVATED BY MANY DRUGS AND DISEASES
81. BIOCHEMICAL MARKERS
• CLINICAL SENSITIVITY FOR ALCOHOL CONSUMPTION SATISFACTORY
• NOT SPECIFIC FOR CHRONIC ALCOHOL ABUSE
ETHYL ESTERS OF FATTY ACIDS
COVALENT PROTEIN ADDUCTS-
• ETHANOL METABOLISM AND LIPID PEROXIDATION
82. BIOCHEMICAL MARKERS
• ALCOHOL INTERFERES WITH GLYCOCONJUGATION REACTIONS -ACETALDEHYDE
INHIBITION OF GLYCOTRANSFERASES
ISOFORMS OF TRANSFERRIN
• CHRONIC ABUSE-CARBOHYDRATE DEFICIENT(CDT) ISOFORMS(HYPOSIALYL AND
ASIALYLTRANSFERRIN)
• CDT AND GGT-INCREASES THE ACCURACY OF DETECTING PROLEM DRINKERS
83. ↑MEAN ERYTHROCYTE CORPUSCULAR VOLUME
• DYSFUNCTIONAL PRODUCTION OF RED CELLS
• MORE SPECIFIC THAN GGT
• PT PROLONGED
• DECREASED ALBUMIN
SERUM LEVELS OF PROCOLLAGEN TYPE III
• CORRELATE WITH COLLAGEN SYSTHESIS
• DISEASE SEVERITY
84. NON SPECIFIC LAB ABNORMALITIES
• HYPERURICEMIA
• HYPERLACTICACIDEMIA
• HYPERTRYGLYCERIDEMIA
• HYPOGLYCEMIA
• HYPERGLYCEMIA
• HYPOPHOSPHATEMIA
• HYPOMAGNESEMIA
• MACROCYTOSIS
Liver biopsy
•Disease severity
•Prognosis
•Rule out
treatable diseases
like chronic
hepatitis and
hemochromatosis
85. ACUTE ALCOHOLIC HEPATITIS
DISCRIMIANT FUNCTION
• [4.6X(PT-CONTROLPT)]+PLASMA BILIRUBIN(MG/DL)] VALUE >32
• HIGH MORTALITY RATE
MODEL FOR END STAGE LIVER DISEASE(MELD)SCORE>11
• SIMILAR SENSITIVITY
• BETTER SPECIFICITY