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Questions and Answers
What should be the first priority in the management of a patient with ethanol poisoning?
What should be the first priority in the management of a patient with ethanol poisoning?
Which of the following is NOT a recommended treatment approach for severe ethanol intoxication?
Which of the following is NOT a recommended treatment approach for severe ethanol intoxication?
What is the primary source of methanol exposure in humans?
What is the primary source of methanol exposure in humans?
How does methanol primarily cause toxicity in the body?
How does methanol primarily cause toxicity in the body?
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Which treatment is specifically indicated for hypoglycemia in cases of ethanol poisoning?
Which treatment is specifically indicated for hypoglycemia in cases of ethanol poisoning?
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What metabolic disturbance is a significant concern in methanol poisoning?
What metabolic disturbance is a significant concern in methanol poisoning?
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What characteristic makes methanol metabolism slower compared to ethanol?
What characteristic makes methanol metabolism slower compared to ethanol?
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Which of the following antidotes can accelerate the metabolism of ethanol?
Which of the following antidotes can accelerate the metabolism of ethanol?
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What blood alcohol level is typically considered legally intoxicated?
What blood alcohol level is typically considered legally intoxicated?
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What is a common clinical presentation at a blood alcohol level of 0.15 - 0.3%?
What is a common clinical presentation at a blood alcohol level of 0.15 - 0.3%?
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Which symptom indicates severe toxicity from ethanol at blood alcohol levels over 0.5%?
Which symptom indicates severe toxicity from ethanol at blood alcohol levels over 0.5%?
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What is the expected consequence when blood alcohol levels exceed 300 mg/dL in novice drinkers?
What is the expected consequence when blood alcohol levels exceed 300 mg/dL in novice drinkers?
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Which rapid test is not used to assess motor skills in cases of suspected alcohol intoxication?
Which rapid test is not used to assess motor skills in cases of suspected alcohol intoxication?
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What treatment measure is critical in cases of ethanol toxicity?
What treatment measure is critical in cases of ethanol toxicity?
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What blood chemistry change is associated with ethanol intoxication?
What blood chemistry change is associated with ethanol intoxication?
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What is McEwen’s sign indicative of in cases of severe ethanol toxicity?
What is McEwen’s sign indicative of in cases of severe ethanol toxicity?
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Which of the following clinical presentations is most likely associated with severe metabolic acidosis due to methanol toxicity?
Which of the following clinical presentations is most likely associated with severe metabolic acidosis due to methanol toxicity?
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What is the primary reason for using ethanol as an antidote in methanol poisoning?
What is the primary reason for using ethanol as an antidote in methanol poisoning?
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Which method is NOT recommended for gastrointestinal decontamination in cases of methanol poisoning?
Which method is NOT recommended for gastrointestinal decontamination in cases of methanol poisoning?
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In which scenario is hemodialysis indicated for a patient with methanol poisoning?
In which scenario is hemodialysis indicated for a patient with methanol poisoning?
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Which of the following statements about the clinical presentation from methanol toxicity is true?
Which of the following statements about the clinical presentation from methanol toxicity is true?
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What is a significant metabolic consequence of methanol toxicity that could lead to cardiac complications?
What is a significant metabolic consequence of methanol toxicity that could lead to cardiac complications?
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What is the most serious central nervous system complication associated with methanol poisoning?
What is the most serious central nervous system complication associated with methanol poisoning?
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Which laboratory investigation is crucial for assessing optic nerve damage in methanol poisoning?
Which laboratory investigation is crucial for assessing optic nerve damage in methanol poisoning?
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What is the primary method by which ethanol is metabolized in the body?
What is the primary method by which ethanol is metabolized in the body?
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Which of the following conditions is NOT typically associated with ethanol poisoning?
Which of the following conditions is NOT typically associated with ethanol poisoning?
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Which of the following organs is least involved in the metabolism of ethanol?
Which of the following organs is least involved in the metabolism of ethanol?
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What effect does ethanol have on the central nervous system?
What effect does ethanol have on the central nervous system?
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What percentage of ethanol is typically excreted unchanged in the body?
What percentage of ethanol is typically excreted unchanged in the body?
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Ethanol metabolism leads to a significant decrease in which of the following ratios in the liver?
Ethanol metabolism leads to a significant decrease in which of the following ratios in the liver?
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What is a common physiological response triggered by ethanol's peripheral effects?
What is a common physiological response triggered by ethanol's peripheral effects?
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Which of the following is a consequence of ethanol's effect on metabolism?
Which of the following is a consequence of ethanol's effect on metabolism?
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Study Notes
Alcohol - Ethyl Alcohol (Ethanol)
- Ethanol is one of the oldest drugs recognized by humans.
- It is the primary alcohol found in beers, wines, and distilled spirits.
- It is a clear, colorless liquid with a slight pleasant odor.
- Source: Fermentation of sugar.
Uses
- Beverages (e.g., wines, whisky).
- Over-the-counter products (mouthwashes, aftershave lotions, hair sprays, cough & cold preparations).
- Solvent.
Pharmacokinetics of Ethanol
- Absorption: Primarily (80%) from the small intestine, with some (20%) from the stomach and large intestine.
- Distribution: Distributed to all tissues and body fluids, reflecting water content. Passes the blood-brain barrier and placenta.
- Metabolism: 90-98% removed by enzymatic oxidation, primarily in the liver, with some in the kidneys.
- Excretion: 2-10% excreted unchanged through urine and breath. Small amounts detectable in sweat, tears, bile, and gastric juices.
Conditions of Poisoning
- Accidental: Addicts, children, workers.
- Homicidal: Used to facilitate rape & robbery (similar to barbiturates).
- Suicidal: Rare.
Mechanism of Action
- CNS: Ethanol depresses the central nervous system by impacting neuronal membrane function (possibly via inhibition of Na -K-ATP). The effect is directly proportional to blood concentration.
- Peripheral: Causes vasodilation, leading to a false sensation of warmth. Central thermal auto-regulation is compromised, potentially resulting in lower body temperatures.
- Consequences of Ethanol Metabolism
- Significant decrease in NAD/NADH ratio in the liver
- Inhibits gluconeogenesis
- Reduced glycerol metabolism, leading to fat accumulation in the liver
- Accumulation of Lactic acid & Ketoacids leading to metabolic acidosis
Toxic Dose
- A blood level of 100mg/dL of 0.7g/kg of pure ethanol is considered legally intoxicated.
- Levels sufficient to cause profound coma or respiratory depression are variable, depending on individual tolerance.
- Chronic alcoholics may recover with levels of 500-600mg/dL or higher, while this typically induces coma in novice drinkers.
Clinical Presentation - Stages of Intoxication
- Mild Toxicity (Excitation): Blood alcohol level 0.05% - 0.15%. Symptoms include talkativeness, behavioral changes and euphoria. Centers controlling judgment and behavior are inhibited.
- Moderate Toxicity (Incoordination): Blood alcohol level 0.15% - 0.3%. Symptoms include impaired motor coordination (staggering gait), tremors, slurred speech, decreased motor skills, hiccups, diplopia, vomiting, and flushed skin.
- Severe Toxicity (Seizures & Coma): Blood alcohol level > 0.5%. Symptoms include severe CNS depression (medullary centers), seizures, shock (lowered temperature, blood pressure, rapid/weak pulse, rapid/shallow breathing, alcoholic breath), and may lead to coma and even central asphyxia.
- McEwen sign - Constricted pupil that dilates on pinching the skin of the face or neck.
Investigations
- Rapid tests (finger-to-nose, walking straight lines)
- Chemical analysis (breathalyzer, urine, blood tests)
- Blood chemistry for ketoacidosis
Treatment
- Supportive Measures (ABCs): Prioritize airway, breathing, circulation (oxygen, ventilation as needed).
- GIT Decontamination: Gastric lavage with NaHCO₃ (strong coffee remaining in the stomach after lavage).
- Elimination of Absorbed Poison: Forced alkaline diuresis, or haemodialysis.
- Antidotes (specific): No antidote for Ethanol, but vitamin B1 can stimulate metabolism of ethanol via alcohol dehydrogenase.
- Symptomatic: Treat metabolic acidosis (NaHCO₃), hypoglycemia (10-50% dextrose IV), hypothermia (warming), and shock (expand fluids, use dobutamine).
- Convulsions: Diazepam.
Methyl Alcohol (Methanol) - "Wood Alcohol"
- Methanol is a simpler alcohol, more likely than ethanol to cause serious human toxicity.
- Source: Distillation of wood.
- Uses: Adulterant for ethyl alcohol, solvent, fuel, cleaning agent, etc.
Pharmacokinetics of Methanol
- Absorption: Rapid and complete from the gastrointestinal tract (GIT); inhalation and skin absorption are also possible.
- Distribution: Primarily to the optic nerve.
- Metabolism: 90% in the liver.
- Excretion: Primarily through the liver, with some excretion through the kidneys and lungs. Metabolism is much slower compared to ethanol.
Conditions of Poisoning
- Accidental: Drinking adulterated ethanol, exposure by children or industry workers.
Mechanism of Action
- CNS: Depresses the CNS, but to a greater extent than Ethanol.
- G.I.T: Irritation.
- Metabolic Acidosis: Highly toxic formic acid accumulates due to methanol metabolism, leading to metabolic acidosis. The more toxic formic acid is produced six times faster than methanol, lower ratio of hepatic NAD/NADH resulting in more serious clinical presentation.
- Ocular Toxicity: Formic acid inhibits cytochrome oxidase in the optic nerve, causing cellular ischemia and anaerobic metabolism.
Clinical Presentations
- Visual: Visual impairment (blurring, pain), papilledema, optic atrophy, irreversible blindness (25% of cases).
- Metabolic Acidosis: Moderate to severe with air hunger, confusion, headache, and weakness. Severe cases can lead to life-threatening hyperkalemia.
- Gastrointestinal: Vomiting, abdominal cramps, and dehydration.
- CNS: Disorientation, stupor, coma, convulsions, encephalopathy, breathing issues correlating to severity of acidosis and coma, and shock.
Investigations
- Serum methanol levels
- Fundus examination and visual evoked potential (assessing optic nerve function)
- Arterial blood gas and serum electrolyte analysis to monitor acidosis and hyperkalemia
Treatment
- Supportive Measures (ABCs): Oxygen, airway, breathing, circulation support.
- GIT Decontamination: Gastric lavage (NaHCO₃), noting activated charcoal is ineffective in binding methanol.
- Elimination of Poison: Forced alkaline diuresis, and hemodialysis
- Antidotes: Ethanol (competes with methanol for alcohol dehydrogenase) and 4-methyl pyrazole (blocking methanol metabolism).
- Symptomatic: Metabolic acidosis (NaHCO₃), hypoglycemia (10-50% dextrose IV), hypothermia (warming), shock, convulsions Diazepam.
- Folinic Acid (Leucovorin): Promoting the conversion of formic acid to CO2 & water.
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Description
Explore the fascinating world of ethanol, the primary alcohol found in alcoholic beverages. This quiz covers its properties, uses, pharmacokinetics, and conditions of poisoning. Test your knowledge on this essential compound used throughout history!
