Irreversible inhibitors – Malathion MCQs With Answer

Irreversible inhibitors – Malathion MCQs With Answer

Irreversible inhibitors, especially organophosphates like malathion, are crucial for B.Pharm students to understand due to their clinical, pharmacological, and toxicological importance. This concise, keyword-rich introduction covers mechanism of action (acetylcholinesterase phosphorylation), metabolic activation to malaoxon, factors affecting toxicity, clinical features (SLUDGE, cholinergic crisis), aging, reactivation by oximes, and preventive measures. Emphasis is placed on enzyme kinetics, diagnostic cholinesterase assays, treatment protocols, environmental impact, and regulatory considerations. These concepts help students integrate pharmacology, medicinal chemistry, toxicology, and therapeutics relevant to pesticide exposures. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. Which enzyme is irreversibly inhibited by malathion after metabolic activation?

• Butyrylcholinesterase
• Monoamine oxidase
• Acetylcholinesterase
• Choline acetyltransferase

Correct Answer: Acetylcholinesterase

Q2. Malathion is converted to its more toxic metabolite by which process?

• Hydrolysis by carboxylesterases
• Oxidative desulfuration
• Glucuronidation
• Sulfation

Correct Answer: Oxidative desulfuration

Q3. What is the name of the active toxic metabolite of malathion?

• Malaoxon
• Methoxon
• Malathate
• Malonic acid

Correct Answer: Malaoxon

Q4. Irreversible inhibition of AChE by organophosphates primarily involves formation of which bond with the enzyme?

• Disulfide bond
• Phosphoryl-enzyme bond
• Ionic bond with active site Asp
• Hydrogen bond network

Correct Answer: Phosphoryl-enzyme bond

Q5. Which clinical feature is NOT typically associated with acute organophosphate poisoning?

• Bradycardia
• Miosis
• Hyperreflexia due to nicotinic excess
• Dry skin and mydriasis

Correct Answer: Dry skin and mydriasis

Q6. Which mnemonic summarizes muscarinic signs of organophosphate poisoning?

• SOAP (Salivation, Oliguria, Agitation, Pyrexia)
• SLUDGE (Salivation, Lacrimation, Urination, Defecation, Gastrointestinal upset, Emesis)
• BRAIN (Bradycardia, Respiration issues, Agitation, Incoherence, Nausea)
• FAST (Facial droop, Arm weakness, Speech difficulty, Time)

Correct Answer: SLUDGE (Salivation, Lacrimation, Urination, Defecation, Gastrointestinal upset, Emesis)

Q7. Which antidote is primarily used to reactivate phosphorylated acetylcholinesterase if given early?

• Atropine
• Pralidoxime (2-PAM)
• Diazepam
• Naloxone

Correct Answer: Pralidoxime (2-PAM)

Q8. Which drug is used to treat muscarinic symptoms like bronchorrhea and bronchospasm in organophosphate poisoning?

• Pralidoxime
• Neostigmine
• Atropine
• Propranolol

Correct Answer: Atropine

Q9. “Aging” in organophosphate-inhibited AChE refers to:

• Spontaneous regeneration of AChE over time
• Irreversible loss of an alkyl side chain making reactivation impossible
• Increase in enzyme synthesis in the liver
• Slow renal excretion of the organophosphate

Correct Answer: Irreversible loss of an alkyl side chain making reactivation impossible

Q10. Which laboratory test is most commonly used to assess exposure to malathion?

• Serum acetylcholinesterase activity
• Plasma glucose
• Urine cortisol
• Complete blood count

Correct Answer: Serum acetylcholinesterase activity

Q11. Butyrylcholinesterase (pseudocholinesterase) measurement is useful because:

• It is identical to acetylcholinesterase in function
• It shows earlier and larger changes after organophosphate exposure
• It directly measures central nervous system AChE activity
• It is unaffected by organophosphates

Correct Answer: It shows earlier and larger changes after organophosphate exposure

Q12. Which statement about malathion toxicity in mammals is correct?

• Malathion is highly toxic to mammals without biotransformation
• Mammals detoxify malathion rapidly via carboxylesterases, reducing toxicity
• Malathion acts as a direct cholinergic receptor agonist in mammals
• Malathion accumulates in mammalian adipose tissue indefinitely

Correct Answer: Mammals detoxify malathion rapidly via carboxylesterases, reducing toxicity

Q13. Which structural change increases organophosphate potency as an AChE inhibitor?

• Replacing phosphoryl oxygen with sulfur (thiono) always increases potency
• Addition of bulky alkoxy groups that hinder aging
• Smaller alkyl groups on phosphorus that slow hydrolysis
• None — structure has no impact on potency

Correct Answer: Smaller alkyl groups on phosphorus that slow hydrolysis

Q14. Which route of exposure to malathion is considered most hazardous for systemic poisoning?

• Dermal exposure with intact skin
• Oral ingestion
• Inhalation of high-concentration aerosol
• Ocular exposure with immediate washing

Correct Answer: Oral ingestion

Q15. Which of the following is a delayed neurotoxic effect associated with some organophosphates (OPIDN)?

• Immediate bronchospasm
• Peripheral sensorimotor neuropathy weeks after exposure
• Acute miosis within minutes
• Hepatic necrosis within hours

Correct Answer: Peripheral sensorimotor neuropathy weeks after exposure

Q16. Which group of enzymes contributes to malathion detoxification in insects and mammals?

• CYP450 monooxygenases only
• Carboxylesterases and glutathione-S-transferases
• DNA polymerases
• Proteases

Correct Answer: Carboxylesterases and glutathione-S-transferases

Q17. Which factor reduces efficacy of pralidoxime in reactivating AChE?

• Early administration post-exposure
• Administration before aging occurs
• Aging of phosphorylated enzyme
• Use of appropriate dose and infusion rate

Correct Answer: Aging of phosphorylated enzyme

Q18. Which statement about atropine in organophosphate poisoning is true?

• Atropine reactivates AChE directly
• Atropine antagonizes muscarinic receptors, alleviating secretions and bronchospasm
• Atropine is ineffective for muscarinic symptoms and only treats seizures
• Atropine increases acetylcholine levels by inhibiting cholinesterase

Correct Answer: Atropine antagonizes muscarinic receptors, alleviating secretions and bronchospasm

Q19. Which symptom suggests nicotinic receptor involvement in organophosphate poisoning?

• Miosis
• Bronchospasm
• Muscle fasciculations and weakness
• Excessive salivation

Correct Answer: Muscle fasciculations and weakness

Q20. What is the primary pharmacological difference between carbamates and organophosphates regarding AChE inhibition?

• Carbamates cause irreversible inhibition; organophosphates are reversible
• Carbamates produce transient (reversible) carbamylation, organophosphates produce longer-lasting phosphorylation
• Carbamates only affect peripheral receptors while organophosphates only affect central receptors
• There is no difference in mechanism or duration

Correct Answer: Carbamates produce transient (reversible) carbamylation, organophosphates produce longer-lasting phosphorylation

Q21. Which clinical phase may follow acute organophosphate poisoning and present as muscle weakness after recovery from cholinergic crisis?

• Immediate hypersensitivity phase
• Intermediate syndrome
• Chronic renal syndrome
• Rebound cholinergic crisis

Correct Answer: Intermediate syndrome

Q22. Which compound is used in laboratory assays as a substrate to measure cholinesterase activity?

• Acetylthiocholine
• Glucose-6-phosphate
• Lactate
• Urea

Correct Answer: Acetylthiocholine

Q23. Which precaution is most important for first responders treating malathion-contaminated patients?

• Immediate administration of oximes before decontamination
• Use of personal protective equipment and decontamination to prevent secondary exposure
• Allow patients to remove contaminated clothing in an enclosed ambulance without PPE
• No special measures; malathion is nonhazardous

Correct Answer: Use of personal protective equipment and decontamination to prevent secondary exposure

Q24. Why is pralidoxime less effective after organophosphate-induced AChE aging?

• Pralidoxime is metabolized too slowly
• Aged phosphoryl groups form a stable anionic center that oximes cannot displace
• Atropine blocks pralidoxime action
• Pralidoxime requires acidic pH which aging prevents

Correct Answer: Aged phosphoryl groups form a stable anionic center that oximes cannot displace

Q25. Which organophosphate property increases central nervous system toxicity?

• High polarity and inability to cross BBB
• High lipophilicity allowing BBB penetration
• Large molecular size preventing CNS entry
• Exclusive peripheral receptor selectivity

Correct Answer: High lipophilicity allowing BBB penetration

Q26. Which sign indicates severe cholinergic respiratory compromise requiring intubation?

• Clear lung fields on auscultation
• Respiratory secretions, bronchospasm, and respiratory muscle weakness
• Mild cough with normal oxygenation
• Brisk deep tendon reflexes

Correct Answer: Respiratory secretions, bronchospasm, and respiratory muscle weakness

Q27. Which environmental concern is most associated with widespread malathion use?

• Bioaccumulation in human adipose tissue
• Toxic effects on non-target aquatic organisms and beneficial insects
• Enhancement of groundwater pH
• Permanent soil sterilization

Correct Answer: Toxic effects on non-target aquatic organisms and beneficial insects

Q28. Which pharmacokinetic process activates malathion to malaoxon?

• Hydrolytic cleavage by plasma esterases only
• CYP450-mediated oxidative desulfuration in liver and insects
• Direct conjugation with glucuronic acid
• Photodegradation on plant surfaces only

Correct Answer: CYP450-mediated oxidative desulfuration in liver and insects

Q29. Which clinical intervention is recommended for dermal malathion exposure?

• Immediate application of topical antibiotics only
• Removal of contaminated clothing and copious washing with soap and water
• Encouraging the patient to sleep to recover
• Oral activated charcoal application to the skin

Correct Answer: Removal of contaminated clothing and copious washing with soap and water

Q30. Which cellular mechanism explains muscle weakness in organophosphate poisoning?

• Excess acetylcholine at neuromuscular junction causing depolarization block
• Direct muscle fiber necrosis by organophosphate binding
• Inhibition of calcium release from sarcoplasmic reticulum only
• Absolute deficiency of acetylcholine production

Correct Answer: Excess acetylcholine at neuromuscular junction causing depolarization block

Q31. Which population is particularly at lower risk of severe malathion toxicity due to higher detoxifying enzymes?

• Liver disease patients
• Infants with immature esterases
• Mammals with robust carboxylesterase activity
• Individuals on cholinesterase inhibitors

Correct Answer: Mammals with robust carboxylesterase activity

Q32. Which organophosphate characteristic favors rapid absorption through skin?

• High molecular weight and polarity
• Low lipophilicity and ionic charge
• High lipophilicity and small molecular size
• Strong binding to surface proteins only

Correct Answer: High lipophilicity and small molecular size

Q33. Which measure is NOT part of standard hospital management for severe organophosphate poisoning?

• Airway protection and mechanical ventilation as needed
• High-dose atropine titrated to drying of secretions
• Administration of oximes when indicated
• Routine use of beta-blockers to control bradycardia without atropine

Correct Answer: Routine use of beta-blockers to control bradycardia without atropine

Q34. Which feature differentiates cholinergic crisis from opioid overdose clinically?

• Pinpoint pupils only in cholinergic crisis
• Presence of bronchorrhea, salivation, sweating in cholinergic crisis
• Bradycardia only seen in opioid overdose
• Both conditions are clinically identical

Correct Answer: Presence of bronchorrhea, salivation, sweating in cholinergic crisis

Q35. Which structural element in malathion is essential for organophosphate activity after activation?

• Sulfhydryl group
• Phosphorodithioate moiety
• Carboxylic acid terminal group
• Guanidine side chain

Correct Answer: Phosphorodithioate moiety

Q36. Which clinical laboratory finding supports severe organophosphate poisoning?

• Elevated plasma cholinesterase (pseudocholinesterase) activity
• Markedly reduced RBC acetylcholinesterase activity
• Elevated serum electrolytes only
• Increased hemoglobin concentration due to dehydration

Correct Answer: Markedly reduced RBC acetylcholinesterase activity

Q37. Which antidote is used for seizures caused by organophosphate poisoning?

• Calcium gluconate
• Benzodiazepines like diazepam or midazolam
• Neostigmine
• Antipsychotics

Correct Answer: Benzodiazepines like diazepam or midazolam

Q38. Which is true about occupational exposure limits for malathion?

• There are no regulatory limits because malathion is harmless
• Permissible exposure limits and guidelines exist to minimize inhalational risk
• Only dietary exposure is regulated, not occupational
• Limits are the same worldwide without variation

Correct Answer: Permissible exposure limits and guidelines exist to minimize inhalational risk

Q39. Which monitoring approach is useful in populations suspected of chronic low-level organophosphate exposure?

• Periodic measurement of RBC AChE and plasma cholinesterase activity
• Only annual chest X-rays
• Monitoring serum creatinine exclusively
• Neuroimaging for all exposed individuals weekly

Correct Answer: Periodic measurement of RBC AChE and plasma cholinesterase activity

Q40. Which statement about malathion formulation for public health use is correct?

• Aerosolized high-concentration malathion is preferred for indoor application
• Formulations balance insecticidal efficacy with reduced mammalian toxicity
• All malathion formulations are banned worldwide
• Solid powdered formulations are most commonly used in human homes

Correct Answer: Formulations balance insecticidal efficacy with reduced mammalian toxicity

Q41. Which metabolic reaction reduces malathion toxicity in mammals?

• Oxidative desulfuration to malaoxon
• Hydrolysis by carboxylesterases to inactive diacids
• Conversion to organochlorine derivatives
• Formation of stable AChE complexes

Correct Answer: Hydrolysis by carboxylesterases to inactive diacids

Q42. Which factor can increase susceptibility to organophosphate toxicity?

• Genetic deficiency of plasma carboxylesterase (butyrylcholinesterase)
• Concurrent use of medications that increase carboxylesterase activity
• High dietary antioxidant intake
• Regular exercise routine

Correct Answer: Genetic deficiency of plasma carboxylesterase (butyrylcholinesterase)

Q43. Which mechanism explains why organophosphate poisoning may cause hypoxia?

• Direct inhibition of hemoglobin oxygen-binding site
• Bronchorrhea, bronchospasm, and respiratory muscle paralysis impair ventilation
• Hyperventilation leading to oxygen toxicity
• Excessive erythropoiesis consumes oxygen

Correct Answer: Bronchorrhea, bronchospasm, and respiratory muscle paralysis impair ventilation

Q44. Which is a recommended decontamination measure for ocular exposure to malathion?

• Immediate irrigation with copious water or saline for at least 15 minutes
• Application of vinegar to neutralize the pesticide
• Delay irrigation until hospital arrival
• Use of topical steroids immediately

Correct Answer: Immediate irrigation with copious water or saline for at least 15 minutes

Q45. Which therapeutic strategy may reduce long-term neurological sequelae after severe organophosphate poisoning?

• Delaying atropine administration
• Early aggressive management including airway support, atropine, oximes, and seizure control
• Avoiding oximes to prevent side effects
• Relying solely on supportive care without specific antidotes

Correct Answer: Early aggressive management including airway support, atropine, oximes, and seizure control

Q46. Which statement about malathion’s use in vector control is correct?

• It is ineffective against mosquito larvae
• It is widely used because of relative safety profile and efficacy when formulated correctly
• It causes immediate human fatalities at trace environmental levels
• It never requires environmental risk assessment

Correct Answer: It is widely used because of relative safety profile and efficacy when formulated correctly

Q47. Which factor is most important when selecting an oxime for organophosphate poisoning?

• Ability to cross the blood-brain barrier and reactivate CNS AChE if needed
• Having no affinity for phosphorylated enzyme
• Being an antimuscarinic agent like atropine
• Prolonging the aging process

Correct Answer: Ability to cross the blood-brain barrier and reactivate CNS AChE if needed

Q48. Which clinical pattern suggests a less severe organophosphate exposure?

• Profound respiratory failure and coma
• Isolated mild miosis and transient headache with near-normal cholinesterase
• Persistent muscle weakness requiring ventilation
• Cardiac arrhythmias and refractory hypotension

Correct Answer: Isolated mild miosis and transient headache with near-normal cholinesterase

Q49. Which public health measure reduces risk of malathion poisoning in communities?

• Unregulated application by untrained personnel
• Education on safe handling, proper PPE, and adherence to label instructions
• Encouraging home mixing of concentrated formulations
• Discouraging use of personal protective equipment to save costs

Correct Answer: Education on safe handling, proper PPE, and adherence to label instructions

Q50. Which research topic would best deepen B.Pharm students’ understanding of irreversible inhibitors like malathion?

• Comparative kinetics of AChE phosphorylation and aging for different organophosphates
• Study of unrelated antiviral drug resistance
• Investigation of carbohydrate metabolism in plants
• Design of cosmetic formulations containing malathion

Correct Answer: Comparative kinetics of AChE phosphorylation and aging for different organophosphates

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