Reversible inhibitors – Neostigmine MCQs With Answer

Reversible inhibitors – Neostigmine MCQs With Answer

Neostigmine is a prototypical reversible acetylcholinesterase inhibitor widely covered in B. Pharm curricula. This keyword-rich introduction explains its pharmacology, mechanism (carbamylation of AChE), quaternary ammonium structure, limited CNS penetration, and major clinical uses such as myasthenia gravis management and reversal of non-depolarizing neuromuscular blockade. Important concepts include onset/duration, routes of administration, muscarinic versus nicotinic effects, common adverse effects, and key drug interactions. Understanding these topics helps students master dosing, antidote strategies, and clinical monitoring. Clear knowledge of neostigmine’s profile is essential for exams and practice. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. What is the primary mechanism of action of neostigmine?

• Irreversible inhibition of acetylcholinesterase by phosphorylation
• Reversible inhibition of acetylcholinesterase by carbamylation
• Competitive antagonism at muscarinic receptors
• Inhibition of choline uptake into presynaptic terminals

Correct Answer: Reversible inhibition of acetylcholinesterase by carbamylation

Q2. Which structural feature of neostigmine limits its ability to cross the blood–brain barrier?

• Presence of a tertiary amine
• High lipid solubility
• Quaternary ammonium group
• Large aromatic ring system

Correct Answer: Quaternary ammonium group

Q3. Neostigmine is most useful clinically for which of the following indications?

• Treating Parkinson’s disease dementia
• Reversing non-depolarizing neuromuscular blockade
• Chronic suppression of gastric acid secretion
• Long-term central Alzheimer’s therapy

Correct Answer: Reversing non-depolarizing neuromuscular blockade

Q4. Compared to physostigmine, neostigmine:

• Crosses the blood–brain barrier more readily
• Is less polar and more lipid soluble
• Does not significantly cross the blood–brain barrier
• Is an irreversible acetylcholinesterase inhibitor

Correct Answer: Does not significantly cross the blood–brain barrier

Q5. Which adverse effect is most directly related to excess muscarinic stimulation by neostigmine?

• Muscle weakness
• Bronchospasm and increased bronchial secretions
• Peripheral neuropathy
• Hyperglycemia

Correct Answer: Bronchospasm and increased bronchial secretions

Q6. For reversal of residual neuromuscular blockade at the end of surgery, neostigmine is usually co-administered with:

• Propranolol
• Atropine or glycopyrrolate
• Naloxone
• Succinylcholine

Correct Answer: Atropine or glycopyrrolate

Q7. Neostigmine’s duration of action is best described as:

• Extremely short, a few seconds only
• Short to intermediate, typically minutes to a few hours
• Very long, several days
• Permanently irreversible

Correct Answer: Short to intermediate, typically minutes to a few hours

Q8. Which statement about neostigmine metabolism and elimination is correct?

• It is primarily metabolized in the liver by CYP450 enzymes
• It is excreted largely unchanged by the kidneys
• It is inactivated by plasma cholinesterase rapidly
• It is converted to an active metabolite that crosses the BBB

Correct Answer: It is excreted largely unchanged by the kidneys

Q9. The Edrophonium test used in myasthenia gravis differs from neostigmine because edrophonium:

• Is a long-acting carbamate inhibitor like neostigmine
• Has a very rapid onset and short duration of action
• Is a muscarinic antagonist
• Irreversibly inhibits acetylcholinesterase

Correct Answer: Has a very rapid onset and short duration of action

Q10. Which of the following best explains how neostigmine improves muscle strength in myasthenia gravis?

• Direct agonist action at nicotinic receptors
• Increasing acetylcholine concentration at the neuromuscular junction
• Blocking presynaptic calcium channels
• Stimulating release of acetylcholinesterase

Correct Answer: Increasing acetylcholine concentration at the neuromuscular junction

Q11. Which form of neostigmine administration is commonly used for urinary retention caused by postoperative atony?

• Topical application
• Intravenous or intramuscular injection
• Inhalation aerosol
• Intrathecal infusion

Correct Answer: Intravenous or intramuscular injection

Q12. Neostigmine is classified pharmacologically as a:

• Direct cholinergic agonist
• Carbamate reversible acetylcholinesterase inhibitor
• Organophosphate irreversible inhibitor
• Muscarinic receptor antagonist

Correct Answer: Carbamate reversible acetylcholinesterase inhibitor

Q13. A common sign of neostigmine overdose is:

• Tachycardia and dry mouth
• Diaphoresis, salivation, and miosis
• Hyperthermia and mydriasis
• Constipation and urinary retention

Correct Answer: Diaphoresis, salivation, and miosis

Q14. Neostigmine potentiates the effects of which type of neuromuscular blocker?

• Non-depolarizing blockers like vecuronium
• Depolarizing blocker succinylcholine during phase I block
• Direct-acting muscle relaxants
• It antagonizes non-depolarizing blockers

Correct Answer: It antagonizes non-depolarizing blockers

Q15. Which lab or monitoring parameter is most important after neostigmine administration for reversal of neuromuscular blockade?

• Liver function tests
• Continuous ECG and respiratory monitoring
• Serum glucose measurement
• Platelet count

Correct Answer: Continuous ECG and respiratory monitoring

Q16. Which one of the following is a contraindication to neostigmine use?

• Obstructive ileus without surgical decompression
• Myasthenia gravis with response to therapy
• Urinary retention due to atony
• Reversal of non-depolarizing neuromuscular blockade

Correct Answer: Obstructive ileus without surgical decompression

Q17. The chemical classification of neostigmine indicates it is a carbamate. Carbamylation of AChE results in:

• Permanent enzyme inactivation
• Faster hydrolysis than normal acetylcholine
• Temporary protection of the serine hydroxyl, slowing enzyme regeneration
• Activation of AChE

Correct Answer: Temporary protection of the serine hydroxyl, slowing enzyme regeneration

Q18. Which symptom would most likely indicate nicotinic overstimulation due to excess acetylcholine from neostigmine?

• Bradycardia
• Muscle fasciculations and weakness
• Bronchial secretions
• Diarrhea

Correct Answer: Muscle fasciculations and weakness

Q19. When used for myasthenia gravis, neostigmine dosing is typically adjusted based on:

• Body weight only
• Clinical response and measurement of muscle strength
• Fixed schedule regardless of symptoms
• Serum acetylcholinesterase levels

Correct Answer: Clinical response and measurement of muscle strength

Q20. Which drug interaction is clinically important with neostigmine?

• Aminoglycoside antibiotics can enhance neuromuscular blockade
• Beta-blockers increase acetylcholinesterase activity
• Proton pump inhibitors reduce neostigmine absorption significantly
• Statins potentiate cholinergic effects

Correct Answer: Aminoglycoside antibiotics can enhance neuromuscular blockade

Q21. In distinguishing myasthenic crisis from cholinergic crisis, which test historically used edrophonium would show:

• Worsening weakness in myasthenic crisis
• Improvement in weakness in myasthenic crisis
• No change in either crisis
• Immediate bradyarrhythmia in myasthenic crisis only

Correct Answer: Improvement in weakness in myasthenic crisis

Q22. Which of the following best describes the onset of action of neostigmine when given intravenously?

• Several hours
• Within a few minutes
• Days
• Instantaneous (milliseconds)

Correct Answer: Within a few minutes

Q23. Neostigmine’s inability to cross the BBB makes it less useful for which condition compared to physostigmine?

• Peripheral urinary retention
• Central anticholinergic syndrome (delirium due to anticholinergics)
• Reversal of neuromuscular blockade
• Myasthenia gravis

Correct Answer: Central anticholinergic syndrome (delirium due to anticholinergics)

Q24. Which physiological effect is NOT expected after therapeutic doses of neostigmine?

• Increased intestinal motility
• Pupil constriction (miosis)
• Decreased bronchial secretions
• Increased salivation

Correct Answer: Decreased bronchial secretions

Q25. Which pharmacological property explains why neostigmine can be given orally for myasthenia gravis despite being a quaternary ammonium compound?

• Complete absorption and high lipid solubility
• Some absorption occurs via active transport and oral bioavailability sufficient for therapy
• It is converted to a tertiary amine in the gut
• It is administered as a prodrug that crosses membranes easily

Correct Answer: Some absorption occurs via active transport and oral bioavailability sufficient for therapy

Q26. Which of the following signs would prompt immediate administration of atropine after neostigmine overdose?

• Mydriasis and dry skin
• Severe bradycardia and bronchospasm
• Hypertension and agitation
• Hyperreflexia only

Correct Answer: Severe bradycardia and bronchospasm

Q27. Neostigmine acts at which location to increase acetylcholine action in myasthenia gravis?

• Central synapses in the hippocampus
• Neuromuscular junction (motor end plate)
• Autonomic ganglia exclusively
• Adrenal medulla exclusively

Correct Answer: Neuromuscular junction (motor end plate)

Q28. How does renal impairment affect neostigmine dosing?

• Requires dose reduction or longer dosing intervals
• No adjustment is necessary
• Requires switch to inhaled formulation
• Requires co-administration with a CYP inducer

Correct Answer: Requires dose reduction or longer dosing intervals

Q29. Which of the following is a therapeutic use of neostigmine beyond myasthenia gravis and neuromuscular blockade reversal?

• Treatment of chronic asthma as monotherapy
• Management of postoperative urinary retention and ileus
• Long-term treatment of Alzheimer’s disease
• Prophylaxis of motion sickness

Correct Answer: Management of postoperative urinary retention and ileus

Q30. Which clinical feature helps differentiate cholinergic crisis from myasthenic crisis?

• Presence of dry mouth favors cholinergic crisis
• Excess salivation and sweating favor cholinergic crisis
• Improvement after neostigmine suggests cholinergic crisis
• Both crises are indistinguishable clinically

Correct Answer: Excess salivation and sweating favor cholinergic crisis

Q31. In the context of anesthesia, why is atropine or glycopyrrolate given with neostigmine?

• To potentiate neostigmine’s neuromuscular effects
• To block muscarinic side effects such as bradycardia and bronchospasm
• To increase neostigmine CNS penetration
• To induce gastric emptying

Correct Answer: To block muscarinic side effects such as bradycardia and bronchospasm

Q32. Which receptor subtype mediates the increase in gastrointestinal motility seen with neostigmine?

• Beta-2 adrenergic receptors
• Muscarinic M3 receptors on smooth muscle
• Dopamine D2 receptors
• Nicotinic neuronal receptors exclusively

Correct Answer: Muscarinic M3 receptors on smooth muscle

Q33. Which statement about neostigmine and succinylcholine interaction is most accurate?

• Neostigmine always antagonizes succinylcholine’s action
• Neostigmine can prolong phase II block and should be used cautiously after succinylcholine
• Neostigmine converts succinylcholine into an inactive metabolite
• There is no interaction between neostigmine and succinylcholine

Correct Answer: Neostigmine can prolong phase II block and should be used cautiously after succinylcholine

Q34. Which of the following best describes the clinical monitoring sign of adequate reversal of neuromuscular blockade after neostigmine?

• Return of sustained head lift and adequate tidal volume
• Complete absence of bowel sounds
• Persistent apnea
• Bradyarrhythmia resistant to atropine

Correct Answer: Return of sustained head lift and adequate tidal volume

Q35. Which enzyme is directly inhibited by neostigmine?

• Monoamine oxidase
• Acetylcholinesterase
• Butyrylcholinesterase exclusively
• Dipeptidyl peptidase

Correct Answer: Acetylcholinesterase

Q36. Which adverse cardiovascular effect is most likely after neostigmine administration without antimuscarinic co-treatment?

• Hypertension with tachycardia
• Bradycardia, possibly leading to asystole
• Ventricular fibrillation due to direct myocardial toxicity
• Marked QT prolongation as a primary effect

Correct Answer: Bradycardia, possibly leading to asystole

Q37. The term ‘reversible inhibitor’ for neostigmine indicates that:

• The drug forms a permanent covalent bond with AChE
• The enzyme activity returns after spontaneous hydrolysis of the carbamylated enzyme
• The drug effect cannot be reversed by any means
• The drug acts as a competitive antagonist at muscarinic receptors

Correct Answer: The enzyme activity returns after spontaneous hydrolysis of the carbamylated enzyme

Q38. Which population requires extra caution when using neostigmine due to risk of bronchospasm?

• Patients with chronic obstructive pulmonary disease or asthma
• Patients with hyperthyroidism only
• Patients with controlled hypertension only
• Young healthy athletes

Correct Answer: Patients with chronic obstructive pulmonary disease or asthma

Q39. Which clinical scenario is an appropriate indication for neostigmine administration?

• Prophylaxis of peptic ulcer disease
• Postoperative paralytic ileus in a patient without bowel obstruction
• Acute MI to reduce infarct size
• Treatment of acute anxiety

Correct Answer: Postoperative paralytic ileus in a patient without bowel obstruction

Q40. Neostigmine can be used as an antidote for which of the following poisonings?

• Organophosphate poisoning
• Anticholinergic (e.g., atropine) central overdose, but less effective than physostigmine
• Opioid overdose
• Cyanide poisoning

Correct Answer: Anticholinergic (e.g., atropine) central overdose, but less effective than physostigmine

Q41. Which of the following best describes the onset and duration differences between edrophonium and neostigmine?

• Edrophonium is slower onset and longer duration than neostigmine
• Edrophonium is rapid onset and shorter duration than neostigmine
• They have identical onset and duration
• Neostigmine has instantaneous onset and no duration

Correct Answer: Edrophonium is rapid onset and shorter duration than neostigmine

Q42. Which clinical sign suggests successful treatment of urinary retention with neostigmine?

• Continued anuria despite therapy
• Spontaneous voiding with decreased bladder volume
• Increased abdominal distension
• Worsening fecal impaction

Correct Answer: Spontaneous voiding with decreased bladder volume

Q43. In teaching B. Pharm students, which point is essential when explaining neostigmine pharmacodynamics?

• It irreversibly phosphorylates AChE like organophosphates
• It transiently carbamylates AChE, reducing hydrolysis of acetylcholine
• It directly stimulates GABA receptors centrally
• It increases acetylcholine synthesis by activating choline acetyltransferase

Correct Answer: It transiently carbamylates AChE, reducing hydrolysis of acetylcholine

Q44. Which adverse effect of neostigmine is mediated by muscarinic stimulation in the GI tract?

• Constipation
• Increased intestinal motility and cramps
• Decreased salivation
• Reduced gastric secretions

Correct Answer: Increased intestinal motility and cramps

Q45. Which monitoring is least relevant after administering neostigmine to reverse neuromuscular blockade?

• Respiratory rate and tidal volume
• Neuromuscular transmission tests (TOF ratio)
• Arterial blood gases if respiratory compromise suspected
• Serial liver enzyme tests

Correct Answer: Serial liver enzyme tests

Q46. Which of the following best describes the use of neostigmine in pregnancy?

• Absolute contraindication in all trimesters
• Used with caution when benefits outweigh risks; limited placental transfer due to quaternary structure
• Recommended as first-line to treat hypertension in pregnancy
• Causes teratogenic effects in all cases

Correct Answer: Used with caution when benefits outweigh risks; limited placental transfer due to quaternary structure

Q47. Which of the following best explains why neostigmine may worsen muscle weakness in a cholinergic crisis?

• It decreases acetylcholine levels at the synapse
• Excess acetylcholine causes depolarization block at the neuromuscular junction
• It blocks nicotinic receptors directly
• It causes irreversible damage to muscle fibers

Correct Answer: Excess acetylcholine causes depolarization block at the neuromuscular junction

Q48. Which statement about dosing frequency for oral neostigmine in chronic myasthenia gravis is correct?

• Once-weekly dosing is sufficient
• Doses are often given multiple times daily to match symptom fluctuations
• Continuous infusion is the only effective method
• Dosing is unnecessary after initial loading

Correct Answer: Doses are often given multiple times daily to match symptom fluctuations

Q49. Which clinical intervention is appropriate for severe neostigmine-induced bronchospasm and bronchorrhea?

• Administer intravenous atropine and provide respiratory support
• Give additional neostigmine to counteract bronchospasm
• Administer beta-blocker to control bronchial tone
• Give high-dose opioid analgesics

Correct Answer: Administer intravenous atropine and provide respiratory support

Q50. For B. Pharm students, which statement summarizes why neostigmine remains clinically important?

• It is the only drug that treats all neurological disorders
• It provides a reversible, peripheral enhancement of cholinergic transmission useful in myasthenia gravis, postoperative ileus, urinary retention, and reversal of neuromuscular blockade
• It has no side effects and requires no monitoring
• It is primarily used as a long-term central nervous system stimulant

Correct Answer: It provides a reversible, peripheral enhancement of cholinergic transmission useful in myasthenia gravis, postoperative ileus, urinary retention, and reversal of neuromuscular blockade

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