Direct acting parasympathomimetics – Carbachol MCQs With Answer

Direct acting parasympathomimetics like Carbachol are essential topics in pharmacology for B. Pharm students, focusing on cholinergic agonists that act directly on muscarinic and nicotinic receptors. This concise, student-friendly overview covers Carbachol’s mechanism of action, resistance to cholinesterase, ocular and clinical applications, pharmacokinetics, adverse effects, contraindications, and drug interactions. Understanding Carbachol helps clarify differences between acetylcholine, bethanechol, and pilocarpine, and deepens knowledge of receptor selectivity, therapeutic uses in glaucoma and intraocular procedures, and emergency management with atropine. Clear grasp of these concepts is crucial for exam success and safe pharmacotherapy. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. Which receptor types are directly activated by Carbachol?

• Only muscarinic receptors
• Only nicotinic receptors
• Both muscarinic and nicotinic receptors
• Adrenergic receptors

Correct Answer: Both muscarinic and nicotinic receptors

Q2. Carbachol is resistant to degradation by which enzyme compared to acetylcholine?

• Monoamine oxidase
• Cholinesterase (acetylcholinesterase)
• Catechol-O-methyltransferase
• Peptidases

Correct Answer: Cholinesterase (acetylcholinesterase)

Q3. What is the primary ophthalmic use of Carbachol?

• Treatment of allergic conjunctivitis
• Induction of miosis during intraocular surgery and glaucoma management
• Reduction of ocular infection
• Relief of dry eye syndrome

Correct Answer: Induction of miosis during intraocular surgery and glaucoma management

Q4. Which adverse effect is most directly associated with systemic parasympathomimetic activity of Carbachol?

• Hypertension
• Bronchospasm
• Hyperglycemia
• Mydriasis

Correct Answer: Bronchospasm

Q5. Which drug is the preferred antidote for Carbachol overdose?

• Neostigmine
• Atropine
• Propranolol
• Physostigmine

Correct Answer: Atropine

Q6. Compared to acetylcholine, Carbachol has which of the following properties?

• Less potent at muscarinic receptors and rapidly degraded
• More resistant to enzymatic hydrolysis and longer duration
• Selective beta-adrenergic agonist activity
• Pure nicotinic antagonist

Correct Answer: More resistant to enzymatic hydrolysis and longer duration

Q7. Which of the following best describes Carbachol’s chemical classification?

• Choline ester carbamate
• Alkaloid muscarinic antagonist
• Benzodiazepine derivative
• Synthetic adrenergic agonist

Correct Answer: Choline ester carbamate

Q8. Carbachol’s effect on intraocular pressure (IOP) is mainly due to which mechanism?

• Decreased aqueous humor production via beta receptor blockade
• Increased trabecular outflow by contracting the ciliary muscle
• Vasoconstriction of choroidal vessels
• Direct cytotoxic destruction of ciliary body

Correct Answer: Increased trabecular outflow by contracting the ciliary muscle

Q9. Why is systemic use of Carbachol limited clinically?

• Poor receptor affinity
• Excessive nicotinic and muscarinic side effects when systemic
• Very high cost prevents systemic use
• Lack of therapeutic indications

Correct Answer: Excessive nicotinic and muscarinic side effects when systemic

Q10. Which of the following is NOT a common adverse effect of Carbachol?

• Salivation
• Diarrhea
• Urinary retention
• Bradycardia

Correct Answer: Urinary retention

Q11. Carbachol is commonly administered by which route for ophthalmic use?

• Intravenous injection
• Topical ocular instillation
• Oral tablet
• Subcutaneous injection

Correct Answer: Topical ocular instillation

Q12. In comparison to pilocarpine, Carbachol is characterized by:

• Greater muscarinic selectivity and no nicotinic action
• Both muscarinic and nicotinic actions and greater resistance to cholinesterase
• Pure alpha-adrenergic agonism
• Long-lasting beta-adrenergic blockade

Correct Answer: Both muscarinic and nicotinic actions and greater resistance to cholinesterase

Q13. Which patient condition is a contraindication for Carbachol use?

• Open-angle glaucoma
• Asthma with bronchospasm
• Dry mouth due to radiation
• Neurogenic ileus

Correct Answer: Asthma with bronchospasm

Q14. The miosis produced by Carbachol is primarily due to stimulation of which muscle?

• Iris dilator muscle
• Ciliary muscle
• Iris sphincter (sphincter pupillae) muscle
• Levator palpebrae superioris

Correct Answer: Iris sphincter (sphincter pupillae) muscle

Q15. Carbachol’s nicotinic action can lead to which effect at neuromuscular junctions?

• Muscle relaxation via neuromuscular blockade only at therapeutic ocular doses
• Initial muscle fasciculations followed by potential paralysis at high systemic doses
• Selective smooth muscle relaxation in bronchi
• No effect on neuromuscular junctions

Correct Answer: Initial muscle fasciculations followed by potential paralysis at high systemic doses

Q16. Which statement about Carbachol’s absorption is correct?

• Well absorbed orally and widely used as oral therapy
• Poor oral absorption; primarily used topically in the eye
• Readily crosses the blood-brain barrier after oral dosing
• Absorbed only when given intramuscularly

Correct Answer: Poor oral absorption; primarily used topically in the eye

Q17. A B. Pharm student should note that Carbachol’s duration of action compared to acetylcholine is:

• Shorter than acetylcholine
• Longer than acetylcholine due to cholinesterase resistance
• Identical to acetylcholine
• Dependent solely on route of administration with no enzymatic differences

Correct Answer: Longer than acetylcholine due to cholinesterase resistance

Q18. Interaction of Carbachol with cholinesterase inhibitors (e.g., neostigmine) will likely cause:

• Antagonism of Carbachol’s effects
• Augmentation of cholinergic effects and increased toxicity
• No interaction as Carbachol is unaffected by cholinesterase
• Selective blockade of muscarinic receptors

Correct Answer: Augmentation of cholinergic effects and increased toxicity

Q19. Which lab or vital sign change would you anticipate after systemic Carbachol administration?

• Tachycardia and hypertension
• Bradycardia and hypotension
• Marked hyperglycemia
• Increased serum sodium

Correct Answer: Bradycardia and hypotension

Q20. For intraocular surgery, Carbachol is used to:

• Induce mydriasis for cataract extraction
• Induce miosis to maintain lens position and decrease IOP
• Act as a local anesthetic
• Sterilize the ocular surface

Correct Answer: Induce miosis to maintain lens position and decrease IOP

Q21. Carbachol’s effect on salivary glands is to:

• Decrease salivation due to sympathetic activation
• Increase salivation via muscarinic stimulation
• Have no effect on salivary secretion
• Cause salivary gland atrophy

Correct Answer: Increase salivation via muscarinic stimulation

Q22. Which structural feature of Carbachol confers resistance to cholinesterase?

• Phenyl ring substitution
• Carbamate or carbamoyl ester linkage replacing the acetyl group
• Large lipophilic tail
• Peptide bond

Correct Answer: Carbamate or carbamoyl ester linkage replacing the acetyl group

Q23. Which of the following is a therapeutic advantage of Carbachol over acetylcholine?

• Greater specificity for beta receptors
• Longer duration of action due to enzymatic resistance
• Oral efficacy for systemic use
• No muscarinic side effects

Correct Answer: Longer duration of action due to enzymatic resistance

Q24. When teaching drug interactions, a B. Pharm student should note that Carbachol’s effect is antagonized by which class of drugs?

• Muscarinic antagonists (anticholinergics) such as atropine
• Beta-adrenergic agonists
• Calcium channel blockers
• ACE inhibitors

Correct Answer: Muscarinic antagonists (anticholinergics) such as atropine

Q25. Carbachol’s role in glaucoma therapy is mainly to:

• Increase aqueous humor production to normalize pressure
• Enhance trabecular meshwork outflow and reduce intraocular pressure
• Act as a prostaglandin analog
• Provide neuroprotection to optic nerve via NMDA antagonism

Correct Answer: Enhance trabecular meshwork outflow and reduce intraocular pressure

Q26. Which symptom reflects excessive muscarinic stimulation by Carbachol?

• Mydriasis and dry mouth
• Sweating, salivation, lacrimation, and diarrhea
• Hyperreflexia and hyperthermia
• Insomnia and agitation

Correct Answer: Sweating, salivation, lacrimation, and diarrhea

Q27. Which pharmacokinetic property is true for Carbachol?

• Highly lipophilic and crosses the blood-brain barrier easily
• Poor systemic absorption and limited central nervous system penetration
• Extensive hepatic metabolism via CYP3A4
• Primarily eliminated by enterohepatic recirculation

Correct Answer: Poor systemic absorption and limited central nervous system penetration

Q28. In a question about receptor selectivity, Carbachol would be classified as which type of agonist?

• Full selective muscarinic agonist
• Non-selective cholinergic agonist (muscarinic and nicotinic)
• Pure nicotinic antagonist
• Adrenergic agonist

Correct Answer: Non-selective cholinergic agonist (muscarinic and nicotinic)

Q29. Which monitoring parameter is most important when Carbachol is inadvertently given systemically?

• Serum potassium levels
• Heart rate and respiratory status due to risk of bradycardia and bronchospasm
• Serum albumin concentration
• Visual acuity only

Correct Answer: Heart rate and respiratory status due to risk of bradycardia and bronchospasm

Q30. Carbachol’s clinical use in ophthalmology is least appropriate in which condition?

• Angle-closure glaucoma where miosis may worsen vision
• Open-angle glaucoma for decreasing IOP via increased outflow
• Miosis during cataract surgery
• Diagnostic miotic testing

Correct Answer: Angle-closure glaucoma where miosis may worsen vision

Q31. Which physiologic action would you expect after topical ocular Carbachol?

• Dilation of pupil and relaxation of ciliary muscle
• Miosis and accommodation spasm due to ciliary muscle contraction
• Corneal anesthesia
• Increased tear evaporation

Correct Answer: Miosis and accommodation spasm due to ciliary muscle contraction

Q32. A distinguishing exam point: Carbachol is more likely than pilocarpine to cause which effect?

• Selective muscarinic activation without nicotinic effects
• Nicotine-like effects such as ganglionic stimulation at higher doses
• No ocular activity
• Beta receptor stimulation

Correct Answer: Nicotine-like effects such as ganglionic stimulation at higher doses

Q33. When used with cholinesterase inhibitors, Carbachol may produce which clinical outcome?

• Reduced cholinergic effects due to competitive inhibition
• Excessive cholinergic stimulation and risk of cholinergic crisis
• Enhanced adrenergic tone
• Complete blockade of muscarinic receptors

Correct Answer: Excessive cholinergic stimulation and risk of cholinergic crisis

Q34. Which description best fits Carbachol’s mechanism at the molecular level?

• Allosteric antagonist of muscarinic receptors
• Direct agonist that binds to and activates cholinergic receptors
• Enzyme that degrades acetylcholine
• Competitive inhibitor of endogenous acetylcholine release

Correct Answer: Direct agonist that binds to and activates cholinergic receptors

Q35. In pharmacology exams, Carbachol toxicity is treated primarily by:

• Administering physostigmine
• Giving atropine to block muscarinic effects
• Administering epinephrine as first-line antidote
• Using benzodiazepines to reverse cholinergic activity

Correct Answer: Giving atropine to block muscarinic effects

Q36. Carbachol’s onset of action when applied topically to the eye is typically:

• Very slow (hours)
• Rapid (minutes)
• Delayed by 24 hours
• Dependent on hepatic activation

Correct Answer: Rapid (minutes)

Q37. Which pharmacotherapeutic class does Carbachol belong to?

• Cholinesterase inhibitors
• Direct-acting cholinergic agonists (parasympathomimetics)
• Beta-blockers
• Carbonic anhydrase inhibitors

Correct Answer: Direct-acting cholinergic agonists (parasympathomimetics)

Q38. For exam preparation, which statement is true regarding Carbachol and blood-brain barrier?

• It readily penetrates into CNS causing central effects
• It poorly penetrates the CNS due to ionic charge and hydrophilicity
• It is actively transported into the brain by P-gp
• It converts into a lipophilic metabolite that enters CNS

Correct Answer: It poorly penetrates the CNS due to ionic charge and hydrophilicity

Q39. Which cardiovascular effect is a direct consequence of Carbachol acting on muscarinic receptors?

• Increased AV node conduction
• Bradycardia due to increased vagal tone
• Increased myocardial contractility via beta-1 activation
• Coronary vasodilation mediated by alpha receptors

Correct Answer: Bradycardia due to increased vagal tone

Q40. Which clinical scenario would favor cautious use or avoidance of Carbachol?

• Patient with chronic obstructive pulmonary disease and reactive airways
• Patient with diabetic neuropathy needing miosis
• Young healthy patient undergoing cataract surgery
• Topical ocular use in controlled glaucoma

Correct Answer: Patient with chronic obstructive pulmonary disease and reactive airways

Q41. Which of the following best describes Carbachol’s effect on gastrointestinal tract?

• Decreased secretions and slowed motility
• Increased secretions and increased motility leading to cramps or diarrhea
• Paralysis of GI smooth muscle
• No effect on GI function

Correct Answer: Increased secretions and increased motility leading to cramps or diarrhea

Q42. Which comparative point is correct for Carbachol vs bethanechol?

• Both are choline esters, but bethanechol is more selective for muscarinic receptors and used for urinary retention
• Bethanechol is a nicotinic agonist only
• Carbachol is a beta-adrenergic agonist while bethanechol is alpha-adrenergic
• Both are used systemically as first-line antiarrhythmics

Correct Answer: Both are choline esters, but bethanechol is more selective for muscarinic receptors and used for urinary retention

Q43. Which pharmacology principle explains why Carbachol has prolonged muscarinic effects?

• High first-pass metabolism increases duration
• Resistance to acetylcholinesterase-mediated hydrolysis
• Active metabolite formation with longer half-life
• P-gp mediated renal reabsorption

Correct Answer: Resistance to acetylcholinesterase-mediated hydrolysis

Q44. Which sign is NOT typical of a cholinergic (muscarinic) toxidrome from Carbachol?

• Miosis
• Bronchorrhea and bronchospasm
• Dry skin and mydriasis
• Bradycardia

Correct Answer: Dry skin and mydriasis

Q45. Which drug class would antagonize the ocular effects of Carbachol?

• Topical beta-blockers
• Topical antimuscarinic agents (e.g., tropicamide, atropine)
• Topical prostaglandin analogs
• Topical carbonic anhydrase inhibitors

Correct Answer: Topical antimuscarinic agents (e.g., tropicamide, atropine)

Q46. Carbachol’s nicotinic receptor activation at autonomic ganglia would likely cause:

• Pure parasympathetic activation without sympathetic effects
• Mixed autonomic responses due to simultaneous ganglionic stimulation
• Selective inhibition of sympathetic nervous system only
• No change in autonomic tone

Correct Answer: Mixed autonomic responses due to simultaneous ganglionic stimulation

Q47. For formulation considerations, an ophthalmic Carbachol product should be stored and labeled to indicate:

• Use as an oral solution only
• Topical ocular use with sterility and appropriate concentration for miosis
• Intravenous infusion for systemic cholinergic therapy
• Use as a nasal decongestant

Correct Answer: Topical ocular use with sterility and appropriate concentration for miosis

Q48. What educational point should a B. Pharm student remember about combining Carbachol with beta-blockers?

• Beta-blockers will potentiate Carbachol’s bronchodilation
• Beta-blockers may exacerbate bronchospasm and bradycardia when combined with parasympathomimetics
• No interaction exists between these drug classes
• Combination is indicated to treat asthma

Correct Answer: Beta-blockers may exacerbate bronchospasm and bradycardia when combined with parasympathomimetics

Q49. Which experimental observation supports Carbachol’s classification as a direct-acting agonist?

• Its effects are blocked by atropine and by nicotinic antagonists depending on the tissue
• Its effects require prior conversion to acetylcholine in vivo
• It increases acetylcholinesterase activity
• It acts only after neuronal release of endogenous neurotransmitter

Correct Answer: Its effects are blocked by atropine and by nicotinic antagonists depending on the tissue

Q50. As a final exam-style question, which clinical statement about Carbachol is correct?

• Carbachol is the first-line systemic drug for urinary retention
• Carbachol is mainly used topically in the eye for miosis and glaucoma because systemic use causes widespread cholinergic effects
• Carbachol selectively inhibits muscarinic receptors and is used as an antagonist
• Carbachol is a long-acting adrenergic agonist used for hypotension

Correct Answer: Carbachol is mainly used topically in the eye for miosis and glaucoma because systemic use causes widespread cholinergic effects

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