OP poiosoning

Which antidote works by reactivating the inhibited acetylcholinesterase enzyme, provided it is administered soon after exposure? *

Succinylcholine Atropine Pralidoxime (2-PAM) Diazepam Physostigmine

What is the primary immediate life-saving intervention for a patient in respiratory distress due to OP poisoning? *

Continuous infusion of Diazepam Aggressive intravenous fluid resuscitation Intravenous administration of Pralidoxime Administration of high-flow oxygen and mechanical ventilation Oral activated charcoal administration

Which of the following sets of symptoms is characteristic of the **muscarinic** effects of acute organophosphorus poisoning? *

Hypertension, seizures, and CNS excitation Paralysis of skeletal muscles and respiratory failure Tachycardia, fasciculations, and muscle weakness Miosis, diaphoresis, and bronchorrhea Urinary retention, dry mouth, and blurred vision

A patient presents 48 hours after known OP exposure with progressive distal muscle weakness and paresthesias, but their muscarinic symptoms have resolved. This condition is most likely: *

Rebound cholinergic effect Intermediate Syndrome (IMS) Serotonin syndrome Cholinergic crisis Organophosphate-Induced Delayed Neuropathy (OPIDN)

Which finding is characteristic of **nicotinic** receptor stimulation in severe OP poisoning? *

Muscle fasciculations and weakness Excessive salivation Miosis Bradycardia Increased bronchial secretions

What is the primary mechanism of toxicity for organophosphorus (OP) compounds? *

Inhibition of acetylcholinesterase via competitive binding Irreversible phosphorylation of muscarinic and nicotinic receptors Agonism at GABA-A receptors leading to CNS depression Irreversible inhibition of acetylcholinesterase by covalent bonding Direct damage to the neuronal cell membrane integrity

Which diagnostic test is considered the gold standard for confirming recent, significant exposure to organophosphorus insecticides? *

Urine metabolite analysis (e.g., p-nitrophenol) Arterial blood gas analysis Complete blood count (CBC) Serum cholinesterase (Pseudocholinesterase) activity measurement Red Blood Cell (RBC) acetylcholinesterase activity measurement

The phenomenon known as \\\"aging\\\" in organophosphate poisoning refers to: *

The development of tolerance to atropine therapy. The slow onset of nicotinic effects hours after exposure. The development of delayed polyneuropathy weeks after acute poisoning. The irreversible binding of the OP to the acetylcholinesterase enzyme, making reactivation impossible. The breakdown of the OP into less toxic metabolites.

What is the recommended initial dose of Atropine for severe, life-threatening cholinergic symptoms in an adult? *

1.0 mg intravenously, repeated every 5 minutes until secretions clear 2 mg intramuscularly, given once 5 mg subcutaneously, repeated every 30 minutes 0.1 mg intravenously, repeated every 5 minutes until secretions clear 10 mg orally, as needed

What is the primary role of Atropine in the management of OP poisoning? *

To treat seizures associated with CNS toxicity To accelerate the metabolism of the organophosphate To block the effects of excessive acetylcholine at muscarinic receptors To bind directly to the nicotinic receptors at the neuromuscular junction To prevent the aging of the inhibited enzyme

Why is the use of depolarizing neuromuscular blockers, such as succinylcholine, generally contraindicated in the initial management of severe OP poisoning? *

They increase the rate of acetylcholinesterase aging. They interfere with the action of Pralidoxime. They compete with atropine for receptor sites. They cause dangerous hypotension requiring vasopressors. They can exacerbate muscle paralysis already present due to nicotinic blockade.

🎓 Practice Quiz

Your Information

Pharmacology Tools

Medical Tools