L4. Management of Specific Poisoning

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Questions and Answers

What is the primary mechanism behind visual disturbances in methanol intoxication?

Increased intracranial pressure from acidosis

Decreased blood flow to the retina

Accumulation of formic acid affecting the optic nerve (correct)

Direct optic nerve damage by methanol

Which laboratory finding is characteristic for diagnosing methanol poisoning?

Increased lactate levels

Hypokalemia

Severe anion gap metabolic acidosis (correct)

Elevated blood glucose levels

What is the primary treatment goal when managing a patient with methanol intoxication?

Inhibition of alcohol dehydrogenase to prevent toxic metabolite formation (correct)

Immediate gastric lavage within 24 hours

Administration of intravenous fluids exclusively

Use of activated charcoal for detoxification

When is hemodialysis indicated in cases of methanol overdose?

When serum concentration exceeds 50 mg/dL or visual symptoms are present Signup and view all the answers

What symptom is NOT typically associated with acute methanol intoxication?

Euphoria or heightened mood Signup and view all the answers

Which mechanism describes how benzene induces toxicity at the cellular level?

Covalent binding to cellular components leading to mutations Signup and view all the answers

What are the primary clinical effects associated with chronic exposure to benzene?

Anemia, leukopenia, and thrombocytopenia Signup and view all the answers

What key laboratory data is crucial for diagnosing carbon monoxide poisoning?

Measurement of carboxyhemoglobin concentration Signup and view all the answers

What is the mechanism of toxicity for carbon monoxide?

Reversible binding to hemoglobin's oxygen-binding sites Signup and view all the answers

What supportive care measure should be taken for patients exposed to benzene?

Aspiration caution due to possible CNS involvement Signup and view all the answers

Which of the following is NOT a recognized source of carbon monoxide exposure?

Exposure to electronic cigarette vapor Signup and view all the answers

What leads to neutropenia when exposed to benzene?

Oxidative stress and bone marrow depression Signup and view all the answers

In emergency care, what initial assessment is critical for carbon monoxide exposure?

Pulse oximetry for oxygen saturation Signup and view all the answers

What is a primary mechanism of toxicity associated with ionizing radiation?

Generation of free radicals (ROS) Signup and view all the answers

Which clinical effect is NOT associated with acute radiation syndrome?

Increased appetite Signup and view all the answers

In the context of radiation-induced cancer, what is the role of the p53 gene?

Encodes a tumor suppressor Signup and view all the answers

What symptom differentiates chronic radiation syndrome from acute radiation syndrome?

Cancer development Signup and view all the answers

Which of the following is a preventive measure against the effects of ionizing radiation?

Wearing protective clothing Signup and view all the answers

What is the primary treatment protocol for carbon monoxide poisoning?

Hyperbaric oxygen therapy Signup and view all the answers

Which chemical agent has a mechanism of inducing DNA strand breaks similar to ionizing radiation?

Alkylating agents Signup and view all the answers

What are reactive oxygen species (ROS) primarily known for in the context of toxicology?

Inducing oxidative stress and damaging cells Signup and view all the answers

Which type of radiation is considered non-ionizing?

Ultraviolet radiation Signup and view all the answers

What is the primary route of exposure for carbon monoxide poisoning?

Inhalation Signup and view all the answers

Which metabolic pathway is responsible for converting ethylene glycol to glycoaldehyde?

Alcohol dehydrogenase pathway Signup and view all the answers

What is the most toxic metabolite of glyoxylate during ethylene glycol metabolism?

Oxalic acid Signup and view all the answers

Which vitamin promotes the metabolism of glycolic acid to α-hydroxy-β-ketoadipate?

Thiamine Signup and view all the answers

What is one of the key clinical presentations of phase 2 ethylene glycol intoxication?

Cardiorespiratory toxicity Signup and view all the answers

What laboratory finding is characteristic for ethylene glycol poisoning?

Calcium oxalate crystals in urine Signup and view all the answers

Which of the following describes the latency period between methanol ingestion and onset of toxicity?

Latency due to metabolism of methanol to toxic metabolites Signup and view all the answers

Which metabolite of methanol is primarily responsible for causing metabolic acidosis?

Formic acid Signup and view all the answers

Which condition can result from the renal toxicity of ethylene glycol after 24 to 72 hours of ingestion?

Oliguric renal failure Signup and view all the answers

Which physiological effect is a symptom of phase 1 ethylene glycol intoxication?

Confusion Signup and view all the answers

What is the role of folate in the metabolism of methanol?

Promotes the conversion of formic acid to carbon dioxide Signup and view all the answers

What is the primary mechanism of action of N-Acetylcysteine in acetaminophen toxicity?

Enhancing synthesis of glutathione Signup and view all the answers

When is the optimal time frame for administering N-acetylcysteine to maximize its hepatoprotective effects?

Within 8 hours after ingestion Signup and view all the answers

Which of the following lab tests is NOT part of the assessment for acetaminophen toxicity?

Thyroid function test Signup and view all the answers

What is the implication for patients with acetaminophen plasma levels below the ‘possible’ line on the Rumack-Matthew nomogram?

They can be discharged after medical clearance. Signup and view all the answers

Which statement correctly describes the role of liver transplantation in acetaminophen overdose?

It may be necessary for patients with severe hepatotoxicity. Signup and view all the answers

Which of the following statements about the timing of NAC therapy is accurate?

Late initiation of NAC may still provide benefits in specific cases. Signup and view all the answers

Which of the following is a direct action of N-acetylcysteine in treating acetaminophen toxicity?

Binding directly to NAPQI Signup and view all the answers

What aspect of the Rumack-Matthew nomogram is important for clinical decision-making in acetaminophen overdose?

It helps predict the potential for hepatotoxicity based on plasma levels. Signup and view all the answers

What lab result is typically monitored to assess renal function during acetaminophen management?

Serum creatinine (Scr) Signup and view all the answers

Which of the following describes gastrointestinal decontamination for acetaminophen overdose?

Administering activated charcoal within 1-4 hours post-ingestion. Signup and view all the answers

Study Notes

Management of Specific Poisoning

Objectives: Management of specific poisoning conditions
- Ionizing radiation
- Benzene
- Carbon monoxide
- Cyanide
- Alcohols
- Acetaminophen
- Salicylates/Aspirin

Ionizing Radiation (IR)

Clinical effects: Acute radiation syndrome (N/V, fall in blood count, fever, infection). Chronic radiation syndrome (radiation sickness, cancer)
Mechanism of toxicity: Production of free radicals (ROS). ROS damage DNA through electron scavenging causing DNA strand breaks (irreversible). ROS can induce mutation of the p53 gene leading to increased cancer risk.
Treatment: Primarily supportive, blood transfusions, antibiotics for infection

Aromatic Hydrocarbons- Benzene

Routes of Exposure: Swallowing, inhalation, cigarette smoke
Clinical effects: Irritating to skin, eyes, GI and respiratory tract. Can cause chronic exposure toxicity resulting in anemia, leukopenia, thrombocytopenia and bone marrow depression.
Mechanism of toxicity: Benzene metabolites bind covalently to proteins, DNA, and RNA affecting cells by mutation or apoptosis (human carcinogen). Oxidative stress contributes to benzene toxicity.
Treatment: Supportive care (aspiration caution), no specific antidote

Carbon Monoxide (CO)

Sources: Combustion of fuel, indoor heating, smoke, automobile exhaust
Mechanism of toxicity: CO combines with Hb (220X more affinity that O2) forming carboxyhemoglobin (COHb) blocking O2 transport to tissues, leading to cellular hypoxia(potentially reversible), and damages endothelial cells leading to oxidative injury, impaired myocardial contractility, and lipid peroxidation. Heart and brain most affected
Clinical Effects: Headache, confusion, loss of visual acuity, tachycardia, respiratory difficulty, convulsions, shock, metabolic acidosis, respiratory failure, and death
Treatment: Stop exposure, remove patient (decontamination), maintain respiration, assist ventilation, O2 therapy, possibly hyperbaric O₂ therapy

Cyanide (CN)

Sources: Fumigants, industrial chemicals, nail polish remover, burning plastics, fire
Mechanism of toxicity: Inhibits cellular cytochrome oxidase, blocks aerobic O₂ utilization and forces a shift to anaerobic metabolism, leading to lactic acidosis.
Clinical presentation: Headache, dyspnea, metabolic acidosis, nausea, vomiting, ataxia, coma, seizures, collapse and death
Treatment: Supportive care, 100% oxygen (immediately to all patients), Hydroxocobalamin to bind and detoxify free cyanide forming less-toxic cyanocobalamin (vitamin B12).Sodium nitrite produces cyanide-scavenging methemoglobinemia, and sodium thiosulfate is used to treat cyanide converting it to a less toxic form (thiocyanate)

Alcohol Poisoning

Methanol and Ethylene Glycol: Toxic alcohols often ingested accidentally or as ethanol substitutes
Ethylene glycol: Used as antifreeze found in coolants.
Toxicokinetics (EG): Metabolized by Alcohol Dehydrogenase (ADH) to glycoaldehyde, then to glycolic acid and glyoxylic acid. The final toxic metabolite is oxalic acid, causing kidney damage.
Clinical presentation: CNS depression, nausea/vomiting, ataxia, nystagmus, hallucinations, coma, seizures; followed by cardiorespiratory toxicity(hypotension, tachypnea, congestive heart failure, myositis, pulmonary edema). Renal toxicity (flank pain, oxalate crystalluria, oliguric renal failure).
Lab findings: Severe metabolic acidosis (increased anion gap), hypocalcemia, calcium oxalate crystals in the urine
Treatment: Support, Decontamination, Ethanol (inhibit ADH), correction of acidosis (bicarbonate), and cofactors(like thiamine, pyridoxine). Hemodialysis might be needed for removal of the toxins

Methanol (Wood alcohol)

Sources: Component of perfumes, solvents, brake fluid, windshield washer fluid
Toxicokinetics: Converted to formaldehyde and then formic acid. Formic acid is highly toxic and causes metabolic acidosis
Clinical presentation: Acute presentation with gastrointestinal symptoms, followed by visual disturbances, metabolic acidosis, difficulty breathing, coma or death.
Treatment: Similar to ethylene glycol—supportive care, decontamination, ADH inhibition (ethanol or fomepizole), and bicarbonate for acidosis

Acetaminophen (Paracetamol) Poisoning

High-risk groups: Malnourished, anorexic patients. Liver disease, HIV, chronic alcoholics,
Mechanism of toxicity: Initially metabolized by glucuronidation and sulfation (non-toxic) pathways. However, at high doses CYP2E1 produces NAPQI, a highly reactive metabolite that damages liver tissues through depletion of glutathione.
Toxicokinetics: Well-absorbed in the GI tract and metabolized rapidly in the liver. Less than 5% is excreted unchanged in urine.
Clinical presentation: Initially asymptomatic, then nausea, vomiting, abdominal pain, followed by jaundice, liver failure.
Treatment: Gastric decontamination, supportive care. N-acetylcysteine (NAC) within 8 hours for best outcome.

Salicylates

Sources: Many over-the-counter products (e.g., aspirin).
Mechanism of toxicity: Stimulates respiratory center in the brain causing hyperventilation initially, leading to respiratory alkalosis. Later, causes metabolic acidosis, hypoglycemia, and hypokalemia. Also can affect platelets and cause GI bleeding.
Clinical presentation: Nausea, vomiting, dizziness, tinnitus (mild toxicity); hyperventilation, ataxia and malaise (moderate toxicity); lethargy, seizures, coma, metabolic acidosis, GI bleeding, increased prothrombin time, renal failure, hepatic toxicity, lung injury.
Treatment: Supportive care, decontamination, alkalinization of urine and plasma to increase excretion. Hemodialysis for severe toxicity.

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Description

This quiz focuses on the management of various specific poisoning conditions, including ionizing radiation, benzene, carbon monoxide, cyanide, and alcohols. You will explore clinical effects, mechanisms of toxicity, and treatment strategies for each poison. Test your knowledge and understanding of these critical healthcare topics.