Cholinesterase reactivator – Pralidoxime chloride MCQs With Answer

Pralidoxime chloride is a key cholinesterase reactivator used in managing organophosphate poisoning by regenerating inhibited acetylcholinesterase (AChE) and reversing neuromuscular and muscarinic effects. For B. Pharm students, mastering pralidoxime’s mechanism of action, oxime chemistry, pharmacokinetics, dosing strategies, therapeutic window, adverse effects, and comparisons with other oximes is vital for clinical toxicology and therapeutics. These focused MCQs emphasize AChE inhibition kinetics, aging, dosing regimens, administration routes, contraindications, monitoring, and evidence-based protocols to build strong exam-ready knowledge and clinical reasoning. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. Which molecular action best describes how pralidoxime (2-PAM) reactivates acetylcholinesterase?

• Oxidation of the phosphorylated serine residue
• Nucleophilic attack on the phosphorus atom of inhibited AChE
• Competitive inhibition of acetylcholine at muscarinic receptors
• Covalent alkylation of cholinesterase active site

Correct Answer: Nucleophilic attack on the phosphorus atom of inhibited AChE

Q2. Pralidoxime chloride is most effective when administered within which period after organophosphate exposure?

• Within minutes to a few hours before aging occurs
• Only after 72 hours post-exposure
• Any time, aging does not affect efficacy
• Only prior to exposure as prophylaxis

Correct Answer: Within minutes to a few hours before aging occurs

Q3. The term “aging” in organophosphate-inhibited AChE refers to:

• Spontaneous hydrolysis restoring AChE activity
• Irreversible dealkylation of the phosphorylated enzyme making reactivation difficult
• Detoxification of organophosphate in the liver
• Time-dependent decrease in organophosphate potency

Correct Answer: Irreversible dealkylation of the phosphorylated enzyme making reactivation difficult

Q4. Which pharmacokinetic property of pralidoxime influences the need for continuous infusion in severe poisoning?

• High oral bioavailability
• Short plasma half-life
• Extensive tissue accumulation
• Slow renal excretion causing prolonged action

Correct Answer: Short plasma half-life

Q5. Pralidoxime chloride is classified pharmacologically as a(n):

• Antimuscarinic agent
• Oxime reactivator
• AChE inhibitor
• Benzodiazepine sedative

Correct Answer: Oxime reactivator

Q6. Which of the following routes is commonly used for pralidoxime administration in emergency settings?

• Oral tablet
• Intravenous bolus followed by infusion
• Transdermal patch
• Inhalation aerosol

Correct Answer: Intravenous bolus followed by infusion

Q7. A key difference between pralidoxime and atropine in organophosphate poisoning is:

• Pralidoxime treats muscarinic symptoms while atropine reactivates AChE
• Atropine reverses nicotinic symptoms; pralidoxime blocks acetylcholine receptors
• Pralidoxime reactivates AChE; atropine antagonizes muscarinic receptors
• Both drugs share the same mechanism but different names

Correct Answer: Pralidoxime reactivates AChE; atropine antagonizes muscarinic receptors

Q8. Which laboratory parameter is most directly used to monitor severity and recovery in organophosphate poisoning?

• Plasma glucose
• Serum creatinine
• Red blood cell or plasma acetylcholinesterase activity
• Complete blood count

Correct Answer: Red blood cell or plasma acetylcholinesterase activity

Q9. Which adverse effect is commonly associated with high doses of pralidoxime?

• Bradycardia
• Hypertension and tachycardia
• Severe hypoglycemia
• Prolonged QT interval

Correct Answer: Hypertension and tachycardia

Q10. Which statement about pralidoxime efficacy against carbamate poisoning is correct?

• Pralidoxime is universally effective and always required
• Carbamate-AChE complexes age faster, so pralidoxime is essential
• Pralidoxime may have limited benefit because carbamate inhibition is reversible
• Pralidoxime worsens carbamate toxicity and is contraindicated

Correct Answer: Pralidoxime may have limited benefit because carbamate inhibition is reversible

Q11. The therapeutic goal of pralidoxime administration is to:

• Increase acetylcholine release at synapses
• Restore inhibited acetylcholinesterase activity to reduce acetylcholine accumulation
• Block nicotinic receptors permanently
• Neutralize free organophosphate in blood by binding

Correct Answer: Restore inhibited acetylcholinesterase activity to reduce acetylcholine accumulation

Q12. Which chemical feature of pralidoxime is critical for nucleophilic attack on phosphorylated AChE?

• Quaternary ammonium group only
• Pyridinium oxime moiety
• Sulfhydryl group
• Large lipophilic aromatic ring

Correct Answer: Pyridinium oxime moiety

Q13. Pralidoxime does NOT effectively reverse which of the following symptoms when given late after exposure?

• Excessive salivation (sialorrhea)
• Bronchospasm
• Neuromuscular paralysis due to aged AChE
• Miosis

Correct Answer: Neuromuscular paralysis due to aged AChE

Q14. In poisoning with organophosphates, why are RBC AChE measurements preferred over plasma cholinesterase (butyrylcholinesterase) for assessing neuromuscular recovery?

• RBC AChE more closely reflects synaptic AChE status
• Plasma cholinesterase is more specific to neuromuscular junctions
• RBC AChE is easier to measure rapidly in ED
• Plasma cholinesterase is unaffected by organophosphates

Correct Answer: RBC AChE more closely reflects synaptic AChE status

Q15. Which dosing regimen is a commonly recommended initial IV bolus for adult pralidoxime therapy in severe poisoning?

• 15–30 mg/kg over 30 minutes
• 1 g IV bolus followed by infusion
• 10 mg orally once
• 500 mg IM single dose only

Correct Answer: 1 g IV bolus followed by infusion

Q16. Pralidoxime’s quaternary ammonium structure affects its pharmacology by:

• Enhancing CNS penetration across intact blood–brain barrier
• Limiting CNS penetration, reducing central reactivation
• Conferring strong oral absorption and bioavailability
• Rendering it metabolically stable for weeks

Correct Answer: Limiting CNS penetration, reducing central reactivation

Q17. Which co-therapy is mandatory in symptomatic organophosphate poisoning alongside pralidoxime for symptomatic relief?

• Flumazenil
• Atropine
• Physostigmine
• Beta-blocker

Correct Answer: Atropine

Q18. Obidoxime and pralidoxime differ primarily in:

• Mechanism—obidoxime inhibits AChE, 2-PAM reactivates only receptors
• Oxime structure and relative efficacy against different organophosphates
• Route—obidoxime is only topical
• Both are identical in structure and action

Correct Answer: Oxime structure and relative efficacy against different organophosphates

Q19. Which patient factor most influences pralidoxime dosing adjustments?

• Body temperature
• Renal function
• Prior vaccine status
• Skin color

Correct Answer: Renal function

Q20. In neonates and infants exposed to organophosphates, pralidoxime administration considerations include:

• Same adult dose irrespective of weight
• Avoid pralidoxime due to toxicity—use only atropine
• Weight-based dosing and careful monitoring for adverse effects
• Prefer oral administration over IV

Correct Answer: Weight-based dosing and careful monitoring for adverse effects

Q21. Which laboratory change would you expect immediately after effective pralidoxime therapy in organophosphate poisoning?

• Further decrease in RBC AChE activity
• Increase in RBC AChE activity towards normal
• Marked leukopenia
• Elevated serum potassium

Correct Answer: Increase in RBC AChE activity towards normal

Q22. What is the primary rationale for continuing pralidoxime infusion after initial bolus dose?

• To maintain blockade of muscarinic receptors
• To sustain reactivation of newly synthesized or slowly re-inhibited AChE
• To sedate the patient
• There is no rationale; single bolus is sufficient

Correct Answer: To sustain reactivation of newly synthesized or slowly re-inhibited AChE

Q23. Which organophosphate characteristic predicts a faster “aging” time and reduced pralidoxime efficacy?

• Large molecular size
• Presence of less steric hindrance around phosphoryl group (e.g., dimethyl vs diethyl)
• High water solubility
• Lack of phosphorus atom

Correct Answer: Presence of less steric hindrance around phosphoryl group (e.g., dimethyl vs diethyl)

Q24. Which monitoring sign indicates inadequate atropine therapy rather than pralidoxime failure?

• Persistent muscle weakness with low AChE
• Continued bronchorrhea and pulmonary secretions
• Improved pupil size but persistent paralysis
• Reduction in salivation but worsening fasciculations

Correct Answer: Continued bronchorrhea and pulmonary secretions

Q25. Which statement about pralidoxime chloride stability and storage is accurate for hospital pharmacies?

• Pralidoxime is stable at room temperature for months once diluted
• Reconstituted solutions should be used promptly or stored per manufacturer guidance to avoid degradation
• It is photosensitive and must be stored exposed to light
• Frozen storage is required for all preparations

Correct Answer: Reconstituted solutions should be used promptly or stored per manufacturer guidance to avoid degradation

Q26. In which clinical scenario is pralidoxime least likely to be beneficial?

• Recent organophosphate inhalation within 1 hour
• Long-standing paralysis with lab evidence of aged AChE
• Acute occupational exposure with respiratory distress
• Mass casualty organophosphate ingestion where early treatment is possible

Correct Answer: Long-standing paralysis with lab evidence of aged AChE

Q27. Which of the following is a recognized mechanism by which organophosphates cause central nervous system toxicity that pralidoxime may not fully reverse?

• Excessive peripheral muscarinic receptor activation only
• Excess cholinergic neurotransmission in brain regions, with pralidoxime limited by poor CNS penetration
• Direct DNA damage by organophosphates
• Immunologic hypersensitivity reaction

Correct Answer: Excess cholinergic neurotransmission in brain regions, with pralidoxime limited by poor CNS penetration

Q28. What is a contraindication or precaution for high-dose pralidoxime therapy?

• Severe renal impairment requiring dose adjustment
• Concurrent use with atropine
• Hypersensitivity to benzodiazepines
• Pregnancy always contraindicates pralidoxime

Correct Answer: Severe renal impairment requiring dose adjustment

Q29. In managing organophosphate poisoning, pralidoxime is most important for reversing which receptor-mediated effects?

• Only central GABAergic effects
• Nicotinic receptor-mediated neuromuscular dysfunction
• Serotonergic receptor overstimulation
• Histamine-mediated anaphylaxis

Correct Answer: Nicotinic receptor-mediated neuromuscular dysfunction

Q30. The chloride in pralidoxime chloride refers to:

• A counterion that forms the stable salt for parenteral formulation
• An active chloride moiety that reacts with phosphorylated AChE
• Chloride is an impurity and not part of the drug
• Confers lipid solubility for CNS penetration

Correct Answer: A counterion that forms the stable salt for parenteral formulation

Q31. Which factor most limits pralidoxime’s ability to reverse respiratory failure in severe organophosphate poisoning?

• Poor hepatic metabolism
• Insufficient ability to cross blood–brain barrier and late administration after aging
• Excessive protein binding preventing action
• Antagonism by atropine

Correct Answer: Insufficient ability to cross blood–brain barrier and late administration after aging

Q32. Which statement regarding pralidoxime and seizure control is correct?

• Pralidoxime is an effective anticonvulsant in organophosphate-induced seizures
• Pralidoxime may not control central seizures; benzodiazepines are indicated
• Pralidoxime potentiates diazepam, eliminating need for benzodiazepines
• Pralidoxime is contraindicated when seizures occur

Correct Answer: Pralidoxime may not control central seizures; benzodiazepines are indicated

Q33. Which monitoring parameter helps detect pralidoxime toxicity during infusion?

• Serial measurements of transaminases
• Continuous cardiac monitoring for tachyarrhythmias and blood pressure
• Urine dipstick for ketones
• Serial chest X-rays

Correct Answer: Continuous cardiac monitoring for tachyarrhythmias and blood pressure

Q34. Which of the following best describes pralidoxime’s role in mass casualty organophosphate exposure?

• Not useful—only atropine should be used in mass casualty
• Useful when available; priority triage and early atropine are critical, with pralidoxime for moderate-to-severe cases
• Must be given to everyone regardless of symptoms
• Pralidoxime can be administered orally to all affected

Correct Answer: Useful when available; priority triage and early atropine are critical, with pralidoxime for moderate-to-severe cases

Q35. Which pharmacodynamic interaction is important when pralidoxime is co-administered with neuromuscular blocking agents during ICU care?

• Pralidoxime prolongs nondepolarizing neuromuscular blockers
• Pralidoxime can restore AChE so it may reduce the effectiveness of nondepolarizing blockers and affect weaning
• Pralidoxime inactivates succinylcholine
• No interaction exists

Correct Answer: Pralidoxime can restore AChE so it may reduce the effectiveness of nondepolarizing blockers and affect weaning

Q36. Which statement is correct about pralidoxime dosing in renal impairment?

• No adjustment is necessary—renal excretion is irrelevant
• Doses may need reduction or longer intervals due to decreased clearance
• Pralidoxime is contraindicated in renal disease
• Only oral doses should be used in renal impairment

Correct Answer: Doses may need reduction or longer intervals due to decreased clearance

Q37. Which experimental or clinical evidence supports pralidoxime use in organophosphate poisoning?

• Data show oximes worsen outcomes uniformly
• Evidence indicates oximes can improve survival and neuromuscular function when given early for many organophosphates
• Only animal data exist without any human studies
• Pralidoxime is only historically used with no current evidence

Correct Answer: Evidence indicates oximes can improve survival and neuromuscular function when given early for many organophosphates

Q38. Which clinical sign suggests a predominant nicotinic effect that pralidoxime might help reverse?

• Miosis and bradycardia
• Muscle fasciculations and weakness leading to paralysis
• Excessive lacrimation
• Bronchospasm due to muscarinic activation

Correct Answer: Muscle fasciculations and weakness leading to paralysis

Q39. Which of the following best describes pralidoxime’s action on butyrylcholinesterase (plasma cholinesterase)?

• It has no effect on plasma cholinesterase
• It can reactivate plasma cholinesterase but clinical significance is limited compared to RBC AChE
• It permanently inhibits plasma cholinesterase
• It increases plasma cholinesterase synthesis

Correct Answer: It can reactivate plasma cholinesterase but clinical significance is limited compared to RBC AChE

Q40. Which clinical scenario would prompt immediate pralidoxime administration even before lab confirmation?

• Mild headache after possible exposure with normal vitals
• Patient with pinpoint pupils, bronchorrhea, muscle twitching, and respiratory distress
• History of organophosphate exposure but no symptoms
• Chronic cough unrelated to exposure

Correct Answer: Patient with pinpoint pupils, bronchorrhea, muscle twitching, and respiratory distress

Q41. Which organophosphate structural feature correlates with slower aging, enhancing pralidoxime window of opportunity?

• Dimethyl phosphoryl groups
• Diethyl phosphoryl groups with greater steric hindrance
• Absence of phosphoryl halide
• Highly water-soluble polar groups

Correct Answer: Diethyl phosphoryl groups with greater steric hindrance

Q42. Pralidoxime’s volume of distribution is relatively low because:

• It is highly lipophilic and accumulates in fat
• Its quaternary ammonium structure limits tissue and CNS distribution
• It binds extensively to plasma proteins and tissues
• It is actively transported into neurons

Correct Answer: Its quaternary ammonium structure limits tissue and CNS distribution

Q43. Which is an appropriate step if a patient shows recurrent cholinergic signs after stopping pralidoxime infusion?

• Discontinue all therapy and observe
• Restart pralidoxime infusion and reassess atropine needs
• Administer naloxone
• Give high-dose insulin regimen

Correct Answer: Restart pralidoxime infusion and reassess atropine needs

Q44. Which clinical trial challenge complicates establishing universal pralidoxime dosing guidelines?

• Uniform chemical structure of all organophosphates
• Heterogeneity of organophosphate compounds, exposure routes, and aging kinetics
• Lack of any observational data
• Identical patient responses across populations

Correct Answer: Heterogeneity of organophosphate compounds, exposure routes, and aging kinetics

Q45. In the context of pharmacology teaching, pralidoxime is an important example illustrating:

• Receptor agonism at muscarinic receptors
• Enzyme reactivation and structure–activity relationships of antidotes
• Direct blockade of acetylcholine release
• Gene therapy for enzyme deficiency

Correct Answer: Enzyme reactivation and structure–activity relationships of antidotes

Q46. Which patient population requires extra caution due to possible exaggerated cardiovascular response to pralidoxime?

• Patients with preexisting uncontrolled hypertension or tachyarrhythmias
• Young healthy adults with no comorbidity
• Patients with chronic dermatitis
• Those taking broad-spectrum antibiotics

Correct Answer: Patients with preexisting uncontrolled hypertension or tachyarrhythmias

Q47. Which statement best summarizes the role of pralidoxime in modern clinical toxicology?

• Obsolete and replaced entirely by newer drugs
• Still a mainstay antidote for many organophosphate poisonings when used early and with atropine
• Used only in veterinary medicine
• Only useful as a diagnostic agent

Correct Answer: Still a mainstay antidote for many organophosphate poisonings when used early and with atropine

Q48. When counseling a pharmacy student on preparation, which is correct regarding pralidoxime infusion preparation?

• Mix with concentrated acid to stabilize
• Dilute in compatible IV fluids per manufacturer instructions and label infusion duration
• Do not dilute—administer undiluted vial rapidly
• Combine with other incompatible drugs in same syringe to save time

Correct Answer: Dilute in compatible IV fluids per manufacturer instructions and label infusion duration

Q49. In organophosphate poisoning, which combo provides both symptomatic relief and enzyme reactivation?

• Atropine plus pralidoxime
• Propranolol plus naloxone
• Physostigmine alone
• Antihistamines only

Correct Answer: Atropine plus pralidoxime

Q50. For exam preparation, which study focus will best help B. Pharm students master pralidoxime-related questions?

• Only memorizing brand names
• Understanding mechanism of AChE reactivation, aging kinetics, dosing principles, adverse effects, and clinical algorithms
• Learning unrelated antibiotics
• Focusing solely on oral drug formulations

Correct Answer: Understanding mechanism of AChE reactivation, aging kinetics, dosing principles, adverse effects, and clinical algorithms

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