QCM : Toxicology of Carbon Monoxide, Organophosphates, and Psychotropes — 9 questions

Questions et réponses du QCM

1. What is the primary mechanism by which carbon monoxide (CO) causes toxicity in the human body?

CO causes vasodilation leading to hypotension and tissue ischemia
CO directly damages the DNA in cells leading to apoptosis
CO binds irreversibly to hemoglobin, displacing oxygen and causing hypoxia
CO inhibits cytochrome c oxidase in mitochondria, blocking ATP production

CO binds irreversibly to hemoglobin, displacing oxygen and causing hypoxia

Explication

CO binds to hemoglobin with a much higher affinity than oxygen, forming carboxyhemoglobin, which displaces oxygen and leads to tissue hypoxia. This is the main mechanism of CO toxicity, resulting in hypoxic injury especially in the brain and heart.

2. What level of carboxyhemoglobin (%HbCO) typically indicates poisoning, and what level is often fatal according to the revision sheet?

Less than 15%, generally safe; over 20%, severe risk.
Over 15%, indicates intoxication; over 50%, often fatal.
Over 25%, indicates intoxication; over 70%, often fatal.
There is no specific threshold; it depends on symptoms.

Over 15%, indicates intoxication; over 50%, often fatal.

Explication

Levels above 15% indicate CO intoxication, with levels over 50% often being fatal. These thresholds help clinicians assess severity.

3. Which of the following clinical signs is most characteristic of organophosphate poisoning?

Severe hypertension and tachycardia
Muscarinic symptoms such as salivation, bronchorrhea, and miosis
Tremors and hyperreflexia without autonomic symptoms
Profound sedation and respiratory depression without other signs

Muscarinic symptoms such as salivation, bronchorrhea, and miosis

Explication

Organophosphate poisoning causes inhibition of acetylcholinesterase, leading to an accumulation of acetylcholine. This results in a cholinergic crisis characterized by muscarinic symptoms such as salivation, bronchorrhea, miosis, and others. These are hallmark signs of organophosphate toxicity.

4. Which antidotes are used specifically for organophosphate poisoning?

Naloxone and flumazenil.
Atropine and pralidoxime.
Dextrose and calcium.
Digoxin and atropine.

Atropine and pralidoxime.

Explication

Atropine blocks muscarinic effects, and pralidoxime reactivates cholinesterase; both are specific for organophosphate poisoning.

5. In the management of psychotropic overdose, which antidote is specifically used to reverse benzodiazepine effects?

Naloxone
Atropine
Physostigmine
Flumazenil

Flumazenil

Explication

Flumazenil is a specific antagonist of benzodiazepine receptors and is used to reverse the sedative effects of benzodiazepines in overdose situations. Naloxone is used for opioids, physostigmine for anticholinergic toxicity, and atropine for muscarinic poisoning.

6. What is the main mechanism by which carbon monoxide causes tissue hypoxia?

It directly destroys hemoglobin molecules.
It displaces oxygen from hemoglobin by binding to the heme group.
It causes systemic vasodilation leading to hypotension.
It inhibits cytochrome oxidase in mitochondria.

It displaces oxygen from hemoglobin by binding to the heme group.

Explication

CO binds to hemoglobin with high affinity, displacing oxygen and leading to hypoxia especially in vital tissues.

7. Which of the following symptoms is characteristic of a cholinergic crisis caused by organophosphates?

Dry mouth and mydriasis.
Salivation, bronchorrhea, miosis, and muscle weakness.
Tachycardia and hypertension.
Sedation and respiratory depression.

Salivation, bronchorrhea, miosis, and muscle weakness.

Explication

Cholinergic crisis from organophosphates presents with excessive salivation, bronchorrhea, pinpoint pupils, and muscle weakness.

8. According to the revision sheet, which CNS effects are associated with psychotropic overdose?

Only sedation with no other effects.
Depression, excitation, and potential arrhythmias.
Purely neurological seizures without systemic involvement.
Enhanced cognitive function and alertness.

Depression, excitation, and potential arrhythmias.

Explication

Overdose of psychotropes can cause CNS depression or excitation, and may lead to cardiovascular arrhythmias.

9. What is the approximate reduction in half-life of carboxyhemoglobin when hyperbaric oxygen therapy is used compared to breathing air?

From 320 minutes to about 150 minutes.
From 320 minutes to about 23 minutes.
From 300 minutes to 200 minutes.
It does not change; half-life remains the same.

From 320 minutes to about 23 minutes.

Explication

Hyperbaric oxygen significantly reduces the half-life of HbCO from about 320 minutes in air to approximately 23 minutes, facilitating faster detoxification.

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CO — binding to hemoglobin?

Reversibly binds, displacing oxygen

CO poisoning — primary cause?

Inhalation of incomplete combustion gases.

CO toxicity — mechanism?

HbCO formation causes hypoxia and mitochondrial inhibition

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