Cholinesterase inhibitors – irreversible MCQs With Answer

Cholinesterase inhibitors – irreversible MCQs With Answer introduce B.Pharm students to the pharmacology, toxicology, and clinical management of irreversible cholinesterase inhibitors, primarily organophosphates and nerve agents. This concise, Student-friendly post emphasizes keywords like irreversible cholinesterase inhibitors, acetylcholinesterase inhibition, organophosphates, aging, oximes (pralidoxime), and clinical antidotes to improve exam readiness. Content covers mechanism of covalent phosphorylation, diagnostic enzyme assays (RBC AChE, plasma butyrylcholinesterase), clinical features (muscarinic, nicotinic, CNS), and evidence-based emergency treatment including atropine, oximes and supportive care. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. Which chemical class is most commonly associated with irreversible inhibition of acetylcholinesterase?

• Organophosphates
• Carbamates
• Quaternary ammonium compounds
• Beta-lactams

Correct Answer: Organophosphates

Q2. Irreversible cholinesterase inhibitors produce inhibition primarily by forming which type of bond with the enzyme?

• Hydrogen bond
• Ionic bond
• Covalent phosphorylation of active site serine
• Disulfide bridge

Correct Answer: Covalent phosphorylation of active site serine

Q3. “Aging” of phosphorylated acetylcholinesterase refers to:

• Enzyme degradation in lysosomes
• Spontaneous dealkylation making reactivation by oximes difficult
• Reversible dissociation of inhibitor
• Upregulation of enzyme synthesis

Correct Answer: Spontaneous dealkylation making reactivation by oximes difficult

Q4. Which antidote is used to reactivate phosphorylated acetylcholinesterase if given before aging occurs?

• Atropine
• Pralidoxime (2-PAM)
• Diphtheria antitoxin
• Naloxone

Correct Answer: Pralidoxime (2-PAM)

Q5. Which clinical sign is primarily due to nicotinic receptor overstimulation at the neuromuscular junction?

• Miosis
• Bronchorrhea
• Muscle fasciculations and weakness
• Diaphoresis

Correct Answer: Muscle fasciculations and weakness

Q6. Which symptom is considered muscarinic in organophosphate poisoning?

• Muscle weakness
• Tachycardia
• Bronchospasm and increased bronchial secretions
• Fasciculations

Correct Answer: Bronchospasm and increased bronchial secretions

Q7. Which laboratory assay best reflects acetylcholinesterase activity relevant to neuronal synapses?

• Plasma butyrylcholinesterase (pseudocholinesterase)
• Red blood cell (RBC) acetylcholinesterase
• Serum ALT
• Urine cholinesterase

Correct Answer: Red blood cell (RBC) acetylcholinesterase

Q8. Which organophosphate is notorious for rapid aging, limiting oxime efficacy?

• Malathion
• Parathion
• Soman
• Diazinon

Correct Answer: Soman

Q9. Malathion is less toxic to mammals because:

• It is not an organophosphate
• Mammals rapidly detoxify it via carboxylesterases
• It does not inhibit cholinesterase
• It acts as a competitive reversible inhibitor

Correct Answer: Mammals rapidly detoxify it via carboxylesterases

Q10. Which of the following is a nerve agent rather than an agricultural pesticide?

• Parathion
• Sarin
• Malathion
• Diazinon

Correct Answer: Sarin

Q11. Which clinical mnemonic helps remember muscarinic effects of organophosphate poisoning?

• TACHY
• DUMBBELSS (or SLUDGE)
• FAST
• SOAP

Correct Answer: DUMBBELSS (or SLUDGE)

Q12. Atropine alleviates which of the following in organophosphate poisoning?

• Neuromuscular blockade at nicotinic receptors
• Excessive muscarinic secretions and bronchospasm
• Phosphorylation of AChE
• Enzyme aging

Correct Answer: Excessive muscarinic secretions and bronchospasm

Q13. Which statement about pralidoxime (2-PAM) is correct?

• It blocks muscarinic receptors
• It reactivates phosphorylated acetylcholinesterase if given early
• It increases AChE aging
• It is ineffective against organophosphates

Correct Answer: It reactivates phosphorylated acetylcholinesterase if given early

Q14. Which enzyme hydrolyzes succinylcholine and is inhibited by organophosphates?

• Acetylcholinesterase (AChE)
• Butyrylcholinesterase (plasma cholinesterase)
• Monoamine oxidase
• Choline acetyltransferase

Correct Answer: Butyrylcholinesterase (plasma cholinesterase)

Q15. Which organophosphate requires metabolic activation (bioactivation) to form the active oxon?

• Paraoxon
• Parathion
• Sarin
• VX

Correct Answer: Parathion

Q16. Which clinical finding indicates severe central nervous system involvement in organophosphate poisoning?

• Miosis alone
• Seizures and coma
• Tachycardia
• Localized paresthesia

Correct Answer: Seizures and coma

Q17. Which is the primary molecular target residue phosphorylated by organophosphates in AChE?

• Lysine amino group
• Serine hydroxyl group
• Cysteine thiol group
• Histidine imidazole

Correct Answer: Serine hydroxyl group

Q18. Which test result would you expect in a patient with acute organophosphate poisoning?

• Normal RBC AChE and normal plasma cholinesterase
• Decreased RBC AChE and decreased plasma butyrylcholinesterase
• Elevated plasma cholinesterase activity
• Increased serum creatinine kinase only

Correct Answer: Decreased RBC AChE and decreased plasma butyrylcholinesterase

Q19. Which oxime has been used in many countries as an antidote for organophosphate poisoning alongside atropine?

• Diphenhydramine
• Pralidoxime (2-PAM)
• Propranolol
• Physostigmine

Correct Answer: Pralidoxime (2-PAM)

Q20. Why are carbamate cholinesterase inhibitors generally considered reversible compared to organophosphates?

• They have no affinity for AChE
• They carbamylate AChE but the bond hydrolyzes relatively quickly
• They cause permanent enzyme denaturation
• They act only on muscarinic receptors

Correct Answer: They carbamylate AChE but the bond hydrolyzes relatively quickly

Q21. Which organophosphate is used therapeutically as an anti-tremor agent? (Trick: identify correct class)

• Malathion
• Parathion
• No organophosphate is used clinically for tremor; therapeutic agents are reversible AChE inhibitors or anticholinergics
• Soman

Correct Answer: No organophosphate is used clinically for tremor; therapeutic agents are reversible AChE inhibitors or anticholinergics

Q22. Which management step is most essential immediately for a patient with suspected organophosphate dermal exposure?

• Administer activated charcoal
• Remove contaminated clothing and perform dermal decontamination
• Start insulin infusion
• Give oral atropine

Correct Answer: Remove contaminated clothing and perform dermal decontamination

Q23. Which statement about atropine dosing in organophosphate poisoning is correct?

• Small single dose is sufficient
• Titrate doses until muscarinic signs (bronchorrhea, secretions) are controlled
• Atropine reverses nicotinic paralysis effectively
• Atropine is contraindicated

Correct Answer: Titrate doses until muscarinic signs (bronchorrhea, secretions) are controlled

Q24. Which is a limitation of pralidoxime therapy?

• It worsens muscarinic symptoms
• It cannot cross the blood-brain barrier effectively to reverse central AChE inhibition
• It directly blocks acetylcholine receptors
• It increases enzyme aging

Correct Answer: It cannot cross the blood-brain barrier effectively to reverse central AChE inhibition

Q25. Which organophosphate is particularly persistent in the environment and highly toxic, known as a V-agent?

• Sarin
• VX
• Malathion
• Diazinon

Correct Answer: VX

Q26. Which feature differentiates clinical toxicity of organophosphates from pure muscarinic agonists?

• Presence of nicotinic effects like muscle weakness and fasciculations
• Only GI symptoms occur
• No CNS effects are seen
• Miosis is absent

Correct Answer: Presence of nicotinic effects like muscle weakness and fasciculations

Q27. Which pharmacological property describes pralidoxime?

• Muscarinic antagonist
• AChE reactivator (oxime)
• Cholinergic agonist
• CNS depressant

Correct Answer: AChE reactivator (oxime)

Q28. Which of the following is an effect of organophosphate poisoning on the heart?

• Pure tachycardia always
• Bradycardia due to vagal stimulation and varied ECG changes
• No cardiovascular effects
• Immediate myocardial infarction

Correct Answer: Bradycardia due to vagal stimulation and varied ECG changes

Q29. Which statement about pralidoxime administration timing is true?

• It is equally effective even after prolonged exposure and aging
• Early administration increases the likelihood of successful reactivation of AChE
• It should never be used in organophosphate poisoning
• It causes permanent AChE activation regardless of timing

Correct Answer: Early administration increases the likelihood of successful reactivation of AChE

Q30. Which occupational exposure precaution is most effective to prevent organophosphate poisoning?

• Using personal protective equipment and proper handling procedures
• Relying on smell detection
• Wearing cotton gloves only
• Frequent hand-washing without protective clothing

Correct Answer: Using personal protective equipment and proper handling procedures

Q31. Which molecular change renders phosphorylated AChE resistant to oxime reactivation?

• Phosphorylation reversal
• Aging via loss of an alkyl group from the phosphoryl moiety
• Attachment of a sugar residue
• Proteolytic cleavage of the enzyme

Correct Answer: Aging via loss of an alkyl group from the phosphoryl moiety

Q32. Which of the following is a clinical use of reversible cholinesterase inhibitors (not irreversible organophosphates)?

• Glaucoma and myasthenia gravis treatment
• Insect control
• Nerve agent weaponization
• Antibiotic therapy

Correct Answer: Glaucoma and myasthenia gravis treatment

Q33. Which sign differentiates organophosphate-induced bronchospasm from asthma?

• Presence of fever
• Marked bronchorrhea and copious secretions due to muscarinic overstimulation
• Response to beta-agonists alone
• Isolated wheeze without secretions

Correct Answer: Marked bronchorrhea and copious secretions due to muscarinic overstimulation

Q34. Which enzyme pathway bioactivates some organophosphates to more potent AChE inhibitors?

• Cytochrome P450 oxidative desulfuration to form oxons
• Glutathione conjugation in cytosol
• Glucuronidation in liver
• Proteasomal degradation

Correct Answer: Cytochrome P450 oxidative desulfuration to form oxons

Q35. Which drug is contraindicated as sole therapy in organophosphate poisoning because it does not reverse nicotinic effects?

• Pralidoxime
• Atropine alone without oxime in severe poisoning may leave nicotinic paralysis untreated
• Diazepam
• Beta-blockers

Correct Answer: Atropine alone without oxime in severe poisoning may leave nicotinic paralysis untreated

Q36. Which laboratory value is often used to monitor recovery after organophosphate poisoning?

• RBC acetylcholinesterase activity returning toward baseline
• Serum sodium only
• Urine glucose
• Serum lipase

Correct Answer: RBC acetylcholinesterase activity returning toward baseline

Q37. Which organophosphate is commonly used in suicide attempts in some countries due to high toxicity?

• Malathion (low mammalian toxicity)
• Parathion (or parathion derivatives)
• Succinylcholine
• Atropine

Correct Answer: Parathion (or parathion derivatives)

Q38. Which is a central effect of severe organophosphate exposure?

• Peripheral neuropathy only
• Confusion, seizures, and respiratory depression
• Isolated hypertension
• Renal failure as primary sign

Correct Answer: Confusion, seizures, and respiratory depression

Q39. Which long-term complication can follow acute organophosphate poisoning?

• Organophosphate-induced delayed neuropathy (OPIDN) with distal axonopathy
• Immediate cardiac arrest only
• Permanent improved cholinergic function
• Chronic liver regeneration

Correct Answer: Organophosphate-induced delayed neuropathy (OPIDN) with distal axonopathy

Q40. Which receptor type is primarily responsible for salivation in organophosphate poisoning?

• Nicotinic receptors at NMJ
• Muscarinic M3 receptors at salivary glands
• Beta-2 adrenergic receptors
• Dopamine D2 receptors

Correct Answer: Muscarinic M3 receptors at salivary glands

Q41. Which organophosphate treatment reduces seizure activity in severe poisoning?

• High-dose atropine alone
• Benzodiazepines (e.g., diazepam) in addition to antidotes
• Propranolol
• Oral activated charcoal

Correct Answer: Benzodiazepines (e.g., diazepam) in addition to antidotes

Q42. Which property of an organophosphate increases the risk of inhalation exposure in a chemical incident?

• High vapor pressure and volatility (e.g., sarin)
• High molecular weight solids only
• High aqueous solubility alone
• Inability to aerosolize

Correct Answer: High vapor pressure and volatility (e.g., sarin)

Q43. Which clinical test can be used bedside to support cholinergic crisis diagnosis?

• Edrophonium test (Tensilon) only
• Observation of excessive secretions, miosis, bronchospasm, and muscle fasciculations
• Fasting blood glucose
• Chest X-ray only

Correct Answer: Observation of excessive secretions, miosis, bronchospasm, and muscle fasciculations

Q44. Which statement about organophosphate blood levels and clinical correlation is true?

• Blood levels always correlate precisely with symptom severity
• Clinical signs and cholinesterase activities are more important for management than absolute blood pesticide levels
• Blood levels are irrelevant
• Only urine pH matters

Correct Answer: Clinical signs and cholinesterase activities are more important for management than absolute blood pesticide levels

Q45. Which enzyme deficiency increases sensitivity to succinylcholine and some ester anesthetics and can be inhibited by organophosphates?

• Acetylcholinesterase deficiency
• Butyrylcholinesterase (pseudocholinesterase) deficiency or inhibition
• Monoamine oxidase deficiency
• CYP3A4 deficiency

Correct Answer: Butyrylcholinesterase (pseudocholinesterase) deficiency or inhibition

Q46. Which statement about environmental persistence of organophosphates is correct?

• All organophosphates are highly persistent like organochlorines
• Persistence varies; some are hydrolyzed rapidly while others (e.g., VX) are highly persistent
• They all evaporate immediately
• They are completely inert in soil

Correct Answer: Persistence varies; some are hydrolyzed rapidly while others (e.g., VX) are highly persistent

Q47. Which of these is NOT an expected finding in acute organophosphate poisoning?

• Excessive sweating and lacrimation
• Profuse salivation
• Hyperreflexia and muscle weakness
• Hyperglycemia as a primary isolated sign

Correct Answer: Hyperglycemia as a primary isolated sign

Q48. Which preventive pharmacologic measure has been explored for military protection against nerve agents?

• Pre-treatment with reversible AChE inhibitors like pyridostigmine to occupy the enzyme
• Pre-treatment with high-dose atropine daily
• Administering organophosphates in low doses chronically
• Use of beta-blockers prophylactically

Correct Answer: Pre-treatment with reversible AChE inhibitors like pyridostigmine to occupy the enzyme

Q49. Which factor determines the choice between RBC AChE and plasma butyrylcholinesterase assays in suspected poisoning?

• RBC AChE reflects synaptic AChE inhibition; plasma BChE is more sensitive to recent exposure but less specific
• Only plasma BChE is clinically useful
• RBC AChE is irrelevant
• Urine assay is preferred always

Correct Answer: RBC AChE reflects synaptic AChE inhibition; plasma BChE is more sensitive to recent exposure but less specific

Q50. Which immediate supportive intervention can be life-saving in severe organophosphate-induced respiratory failure?

• Early endotracheal intubation and mechanical ventilation
• Oral hydration only
• Topical ocular antibiotics
• Delayed oxygen administration

Correct Answer: Early endotracheal intubation and mechanical ventilation

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.

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