Organophosphorus compound poisoning – mechanism and treatment MCQs With Answer

Organophosphorus compound poisoning – mechanism and treatment MCQs With Answer

Organophosphorus (OP) poisoning, a critical topic for B. Pharm students, involves acetylcholinesterase inhibition leading to cholinergic overstimulation. Understanding the mechanism—AChE phosphorylation, “aging,” and resultant muscarinic and nicotinic signs—is essential for clinical pharmacology. Key treatments include atropine for muscarinic effects, oximes (pralidoxime) to reactivate phosphorylated AChE if given before aging, decontamination, supportive ventilation, and seizure control. Important keywords: organophosphorus poisoning, acetylcholinesterase inhibition, pralidoxime, atropine, cholinergic crisis, RBC AChE, OPIDN, decontamination, B. Pharm. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. What is the primary biochemical mechanism of organophosphorus compound toxicity?

• Blockade of muscarinic receptors
• Inhibition of acetylcholinesterase by phosphorylation
• Activation of monoamine oxidase
• Inhibition of GABA receptors

Correct Answer: Inhibition of acetylcholinesterase by phosphorylation

Q2. Which laboratory assay best reflects neuronal synaptic acetylcholinesterase inhibition in OP poisoning?

• Plasma pseudocholinesterase (butyrylcholinesterase)
• Urine organophosphate metabolites
• Red blood cell acetylcholinesterase activity
• Serum creatine kinase

Correct Answer: Red blood cell acetylcholinesterase activity

Q3. In organophosphate AChE inhibition, what does “aging” refer to?

• Spontaneous reactivation of AChE
• Irreversible dealkylation of the phosphorylated AChE increasing resistance to oximes
• Gradual clinical recovery over weeks
• Formation of reversible carbamylated AChE

Correct Answer: Irreversible dealkylation of the phosphorylated AChE increasing resistance to oximes

Q4. Which antidote directly reactivates phosphorylated acetylcholinesterase if given before aging occurs?

• Atropine
• Pralidoxime (2-PAM)
• Benzodiazepines
• Physostigmine

Correct Answer: Pralidoxime (2-PAM)

Q5. What is the main pharmacologic action of atropine in OP poisoning?

• Reactivates acetylcholinesterase
• Competitive antagonism of muscarinic receptors
• Inhibits nicotinic receptors at the neuromuscular junction
• Enhances acetylcholine release

Correct Answer: Competitive antagonism of muscarinic receptors

Q6. Which clinical feature is primarily muscarinic in organophosphate poisoning?

• Muscle fasciculations
• Tachycardia
• Bronchorrhea and bronchospasm
• Muscle weakness

Correct Answer: Bronchorrhea and bronchospasm

Q7. Which clinical sign is characteristic of nicotinic receptor overstimulation in OP poisoning?

• Miosis
• Bradycardia
• Muscle fasciculations and weakness
• Hypersalivation

Correct Answer: Muscle fasciculations and weakness

Q8. Which test is most useful for confirming exposure and assessing severity in a clinical lab?

• Serum electrolytes
• Red blood cell acetylcholinesterase activity
• Serum liver enzymes
• Urine sodium

Correct Answer: Red blood cell acetylcholinesterase activity

Q9. Globally, what is the most common route of severe OP poisoning presenting to hospitals (suicidal exposures excluded)?

• Inhalation (spray or vapor) and dermal absorption in occupational settings
• Intravenous injection
• Intramuscular injection
• Transdermal therapeutic patch use

Correct Answer: Inhalation (spray or vapor) and dermal absorption in occupational settings

Q10. When is pralidoxime most effective in organophosphate poisoning?

• Only after atropine dosing is complete
• Only in carbamate poisoning
• When administered early, before significant aging of phosphorylated AChE
• After irreversible nerve death has occurred

Correct Answer: When administered early, before significant aging of phosphorylated AChE

Q11. Which anesthetic agent is relatively contraindicated in a patient with acute OP poisoning due to prolonged effect?

• Propofol
• Succinylcholine
• Sevoflurane
• Midazolam

Correct Answer: Succinylcholine

Q12. The first priority for a patient with dermal OP contamination is:

• Administer intravenous atropine immediately
• Decontaminate by removing clothes and washing skin with soap and water
• Give activated charcoal
• Apply topical antidote to skin

Correct Answer: Decontaminate by removing clothes and washing skin with soap and water

Q13. Which mnemonic correctly lists common muscarinic effects of cholinergic excess?

• DUMBBELSS: Diarrhoea, Urination, Miosis, Bradycardia, Emesis, Lacrimation, Sweating, Salivation
• ABCDE: Airway, Breathing, Circulation, Disability, Exposure
• TACHY: Tremor, Agitation, Cyanosis, Hyperthermia, Yawning
• SLUDGE: Seizures, Lethargy, Urination, Diaphoresis, Gastritis, Emesis

Correct Answer: DUMBBELSS: Diarrhoea, Urination, Miosis, Bradycardia, Emesis, Lacrimation, Sweating, Salivation

Q14. Organophosphate-induced delayed neuropathy (OPIDN) is primarily due to inhibition of which target?

• Nicotinic acetylcholine receptor upregulation
• Neuropathy target esterase (NTE) leading to distal axonopathy
• Direct demyelination by atropine
• Excessive acetylcholinesterase activity

Correct Answer: Neuropathy target esterase (NTE) leading to distal axonopathy

Q15. Clinical endpoints for adequate atropinization include:

• Resolution of miosis only
• Heart rate below 40 bpm
• Drying of bronchial secretions, improved air entry, and stable hemodynamics
• Complete normalization of RBC AChE

Correct Answer: Drying of bronchial secretions, improved air entry, and stable hemodynamics

Q16. A commonly used initial IV dose of pralidoxime for an adult with severe OP poisoning is:

• 0.1 mg
• 1–2 g IV bolus (approximately 30 mg/kg), repeat or infusion as needed
• 10 g orally
• 100 units per kg subcutaneously

Correct Answer: 1–2 g IV bolus (approximately 30 mg/kg), repeat or infusion as needed

Q17. How do oximes such as pralidoxime reactivate inhibited AChE?

• They block muscarinic receptors
• They cleave the bond between the phosphate group and the serine hydroxyl of AChE via nucleophilic attack
• They increase acetylcholine synthesis
• They degrade organophosphate compounds in the bloodstream

Correct Answer: They cleave the bond between the phosphate group and the serine hydroxyl of AChE via nucleophilic attack

Q18. Which measurement correlates best with clinical severity and recovery in acute OP poisoning?

• Serum glucose
• Red blood cell acetylcholinesterase activity
• Serum creatinine
• Urine output

Correct Answer: Red blood cell acetylcholinesterase activity

Q19. How do carbamate pesticides differ pharmacologically from organophosphates?

• Carbamates irreversibly phosphorylate AChE
• Carbamates reversibly carbamylate AChE producing shorter duration of inhibition
• Carbamates are potent nicotinic agonists only
• Carbamates cause aging faster than all organophosphates

Correct Answer: Carbamates reversibly carbamylate AChE producing shorter duration of inhibition

Q20. Which drug class is important for controlling seizures in severe OP poisoning?

• Beta-blockers
• Benzodiazepines (e.g., diazepam, lorazepam)
• Typical antipsychotics
• High-dose atropine alone

Correct Answer: Benzodiazepines (e.g., diazepam, lorazepam)

Q21. Which of the following pesticides is NOT an organophosphate?

• Parathion
• Malathion
• Carbaryl
• Diazinon

Correct Answer: Carbaryl

Q22. Chronic low-dose exposure to organophosphates is most associated with which long-term effect?

• Immediate respiratory arrest
• Persistent neurobehavioral deficits and risk of delayed neuropathy
• Permanent hypercholinergic state reversible in hours
• Increased RBC production

Correct Answer: Persistent neurobehavioral deficits and risk of delayed neuropathy

Q23. The most common immediate cause of death in severe OP poisoning is:

• Renal failure
• Respiratory failure due to central respiratory depression, bronchospasm, and secretions
• Sudden myocardial infarction
• Severe hyperthermia

Correct Answer: Respiratory failure due to central respiratory depression, bronchospasm, and secretions

Q24. Arterial blood gases in a patient with hypoventilation from OP-induced respiratory muscle weakness most likely show:

• Respiratory alkalosis
• Metabolic alkalosis
• Respiratory acidosis with hypercapnia
• Normal gases

Correct Answer: Respiratory acidosis with hypercapnia

Q25. Which chest finding is commonly associated with severe OP poisoning?

• Pleural effusion only
• Aspiration pneumonitis and pulmonary edema due to secretions and bronchospasm
• Isolated pneumothorax
• Interstitial fibrosis immediately on exposure

Correct Answer: Aspiration pneumonitis and pulmonary edema due to secretions and bronchospasm

Q26. Concerning carbamate poisoning, which statement about oxime therapy is correct?

• Oximes are essential and always lifesaving in carbamate poisoning
• Oximes are generally unnecessary because carbamylation is reversible and short-lived
• Oximes permanently block muscarinic receptors
• Oximes worsen carbamate toxicity in all cases

Correct Answer: Oximes are generally unnecessary because carbamylation is reversible and short-lived

Q27. Which type of organophosphate tends to undergo “aging” more rapidly, reducing oxime efficacy sooner?

• Diethyl-organophosphates
• Dialkyl phosphorothioates with very long chains
• Dimethyl-organophosphates
• Compounds that are not phosphorylating agents

Correct Answer: Dimethyl-organophosphates

Q28. A commonly recommended initial IV bolus dose of atropine for an adult with severe OP poisoning is:

• 2 mg, repeating and doubling every 3–5 minutes until clinical atropinization
• 0.02 mg once
• 20 mg subcutaneously only
• No atropine should be used

Correct Answer: 2 mg, repeating and doubling every 3–5 minutes until clinical atropinization

Q29. Which clinical sign is the best practical indicator for tapering and stopping atropine therapy?

• Complete normalization of red blood cell AChE levels
• Absence of bronchial secretions, adequate ventilation, and stable hemodynamics
• Return of miosis only
• Patient report of decreased headache

Correct Answer: Absence of bronchial secretions, adequate ventilation, and stable hemodynamics

Q30. Which prophylactic drug has been used to protect against nerve agent exposure by reversible AChE inhibition?

• Pyridostigmine bromide
• Pralidoxime prophylaxis orally
• High-dose atropine daily
• Beta-blockers

Correct Answer: Pyridostigmine bromide

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

Mail- Sachin@pharmacyfreak.com