Ester Local Anesthetics — MCQs
Which of the following local anesthetics is the most common cause of methemoglobinemia?
Mechanism of action of d-tubocurarine is:
Which of the following is a long-acting local anesthetic with a duration of action greater than 2 hours?
A patient presented with rigidity, tremors, and trismus after being administered an anesthetic agent. Which anesthetic agent is most likely to have been administered?
In ophthalmology, if a patient is allergic to aminoesters, which local anesthetic can be safely used?
What is the mechanism of action of local anesthetics?
An 18 years old woman in the active stage of labour requests an epidural anaesthesia for delivery. Immediately following the epidural injection of 12ml of 2% lidocaine, the patient complains of lip numbness and becomes apprehensive. What is the presumptive diagnosis?
Which intravenous anaesthetic agent has analgesic effect also
A patient undergoing a minor surgical procedure is given lignocaine injection. Assertion: Local anaesthetics act by blocking nerve conduction. Reason: Small fibers and non-myelinated fibers are blocked more easily than large myelinated fibers.
Which is correct about the anesthetic drugs X and Y in the image shown? (Recent NEET Pattern 2016-17)
Ester Local Anesthetics Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following local anesthetics is the most common cause of methemoglobinemia?
- A. Lignocaine
- B. Benzocaine (Correct Answer)
- C. Chloroprocaine
- D. EMLA Cream (Lignocaine + Prilocaine)
- E. Prilocaine
- F. Dibucaine
Explanation: ***Benzocaine***- **Benzocaine** is an ester-type local anesthetic that is the **most common cause of methemoglobinemia** among local anesthetics, especially when used in high doses or on mucous membranes due to its rapid absorption.- Its metabolic byproducts, particularly **aniline derivatives**, are potent oxidizers of hemoglobin, converting the ferrous iron (Fe2+) to ferric iron (Fe3+), thus forming methemoglobin which cannot bind oxygen.- **FDA warnings** have been issued regarding benzocaine-induced methemoglobinemia, particularly with topical spray preparations.*Lignocaine*- **Lignocaine** (lidocaine) is an amide-type local anesthetic and is **rarely associated** with methemoglobinemia.- While it can theoretically cause it in very high doses, it is significantly **less potent** in this regard compared to benzocaine.*Chloroprocaine*- **Chloroprocaine** is an ester-type local anesthetic with a very **short duration of action** due to rapid hydrolysis by plasma cholinesterases.- This rapid metabolism typically limits systemic exposure and makes it an **uncommon cause** of methemoglobinemia despite being an ester.*Prilocaine*- **Prilocaine** is an amide-type local anesthetic that can also cause methemoglobinemia, particularly at **higher doses (>600mg)** [1, 2].- It works through its metabolite, **o-toluidine**, which is an oxidizing agent [1].- However, **benzocaine** is more consistently linked to this adverse effect in clinical practice and has more documented case reports.
Question 2: Mechanism of action of d-tubocurarine is:
- A. Competitive, nondepolarizing block at the Nm cholinergic receptor (Correct Answer)
- B. Noncompetitive, depolarizing block at the Nm cholinergic receptor
- C. Non-competitive, nondepolarizing block at the Nm cholinergic receptor
- D. Competitive, depolarizing block at the Nm cholinergic receptor
Explanation: ***Competitive, nondepolarizing block at the Nm cholinergic receptor*** - **d-tubocurarine** acts as a **competitive antagonist** at the **nicotinic muscle (Nm) cholinergic receptors** on the motor endplate. - It competes with **acetylcholine (ACh)** for binding sites, preventing ACh from activating the receptor and causing **muscle paralysis** without depolarization. *Noncompetitive, depolarizing block at the Nm cholinergic receptor* - This describes the mechanism of action of **depolarizing neuromuscular blockers** like **succinylcholine**, which first *depolarize* the motor endplate before causing paralysis. - d-tubocurarine does not cause initial depolarization; it directly blocks the receptor. *Non-competitive, nondepolarizing block at the Nm cholinergic receptor* - While d-tubocurarine is **nondepolarizing**, it is a **competitive antagonist**, not a non-competitive one. - A non-competitive block would involve binding to a different site on the receptor or an associated ion channel, altering receptor function indirectly. *Competitive, depolarizing block at the Nm cholinergic receptor* - This option incorrectly combines the concepts, as **depolarizing blockers** like succinylcholine act initially by **depolarizing** the endplate, whereas d-tubocurarine is purely a **nondepolarizing** agent. - The "competitive" aspect would be true for the binding of ACh to its site on a depolarizing agent, but the effect of d-tubocurarine is simply to block, not depolarize.
Question 3: Which of the following is a long-acting local anesthetic with a duration of action greater than 2 hours?
- A. Bupivacaine (Correct Answer)
- B. Tetracaine
- C. Etidocaine
- D. Prilocaine
Explanation: ***Bupivacaine*** - **Bupivacaine** is an amide-type local anesthetic known for its **long duration of action**, typically lasting 2-8 hours, making it suitable for prolonged pain control. - Its **high lipid solubility** and **protein binding** contribute to its extended effect by increasing tissue penetration and reducing systemic absorption. *Prilocaine* - **Prilocaine** is an intermediate-acting local anesthetic with a duration of action of approximately 1-2 hours. - It is associated with a risk of **methemoglobinemia** in higher doses, less common with other local anesthetics. *Etidocaine* - While considered a long-acting local anesthetic, **Etidocaine** generally has a slightly shorter duration of action compared to bupivacaine, typically 2-6 hours. - It is known for its **rapid onset** and high potency. *Tetracaine* - **Tetracaine** is an ester-type local anesthetic with a duration of action of about 2-3 hours and is primarily used for **spinal anesthesia** and topical applications due to its toxicity for peripheral nerve blocks. - Ester-type local anesthetics like tetracaine are more prone to causing **allergic reactions** due to their metabolism into PABA (para-aminobenzoic acid).
Question 4: A patient presented with rigidity, tremors, and trismus after being administered an anesthetic agent. Which anesthetic agent is most likely to have been administered?
- A. Halothane (Correct Answer)
- B. Nitrous Oxide (N2O)
- C. Thiopentone sodium
- D. Etomidate
Explanation: ***Halothane*** - The combination of **rigidity**, **tremors**, and **trismus** after an anesthetic agent suggests **malignant hyperthermia (MH)**, a rare but life-threatening inherited condition. - **Halothane (and other volatile anesthetics)**, along with succinylcholine, are known triggers for malignant hyperthermia. *Nitrous Oxide (N2O)* - While an anesthetic agent, **nitrous oxide** is not a known trigger for **malignant hyperthermia**. - It works by modulating **NMDA receptors** and does not typically cause rigidity, tremors, or trismus as a side effect. *Thiopentone sodium* - **Thiopentone sodium** is a **barbiturate** anesthetic and is not associated with triggering **malignant hyperthermia**. - Its effects primarily involve potentiation of **GABA-A receptors**, leading to sedation and hypnosis. *Etomidate* - **Etomidate** is a short-acting intravenous anesthetic that is not a known trigger for **malignant hyperthermia**. - It is typically associated with minimal cardiovascular depression but can cause **adrenocortical suppression** with prolonged use.
Question 5: In ophthalmology, if a patient is allergic to aminoesters, which local anesthetic can be safely used?
- A. Procaine
- B. Cocaine
- C. Prilocaine (Correct Answer)
- D. Tetracaine
Explanation: **Local anesthetics are classified into two chemical groups: esters (aminoesters) and amides. Allergies to esters typically do not cross-react with amides.** ***Prilocaine*** - **Prilocaine** is an **amide-type local anesthetic**, and allergies to **aminoesters** typically do not cross-react with **amides**. - It is a safe alternative in patients with a known allergy to **ester-type local anesthetics**. *Cocaine* - **Cocaine** is an **ester-type local anesthetic**, sharing a similar chemical structure with **aminoesters**. - Patients allergic to **aminoesters** are likely to experience a **cross-reaction** with **cocaine**. *Procaine* - **Procaine** is a classic **ester-type local anesthetic** (an aminoester). - An allergy to aminoesters directly implies an allergy to **procaine** due to its chemical classification. *Tetracaine* - **Tetracaine** is also an **ester-type local anesthetic** (an aminoester). - It is contraindicated in patients with an allergy to **aminoesters** due to the high risk of **allergic reaction**.
Question 6: What is the mechanism of action of local anesthetics?
- A. Block chloride channels
- B. Block calcium channels
- C. Block sodium channels (Correct Answer)
- D. Block potassium channels
Explanation: ***Block sodium channels*** - Local anesthetics work by **reversibly binding** to the alpha subunit of **voltage-gated sodium channels** on the neuronal membrane. - This binding prevents the influx of sodium ions, thereby inhibiting the **depolarization** of the neuron and **propagation of action potentials**. *Block chloride channels* - **Chloride channels** are primarily involved in **hyperpolarization** or stabilization of the resting membrane potential, and their blockade is not the primary mechanism of local anesthesia. - Drugs like **benzodiazepines** modulate GABA-gated chloride channels for their anxiolytic and sedative effects. *Block calcium channels* - **Calcium channels** are important for neurotransmitter release and muscle contraction, but their blockade is not the way local anesthetics exert their effects. - **Calcium channel blockers** are used in cardiovascular medicine (e.g., diltiazem, verapamil) to reduce heart rate and blood pressure. *Block potassium channels* - **Potassium channels** are crucial for repolarization of the neuronal membrane and maintaining the resting potential. - While some toxins block potassium channels, it is not the principal mechanism by which **local anesthetics** achieve their nerve blocking effect.
Question 7: An 18 years old woman in the active stage of labour requests an epidural anaesthesia for delivery. Immediately following the epidural injection of 12ml of 2% lidocaine, the patient complains of lip numbness and becomes apprehensive. What is the presumptive diagnosis?
- A. Allergy to drug administered
- B. Systemic toxicity to drug administered (Correct Answer)
- C. Vasovagal shock
- D. Drug entered SA space
Explanation: ***Systemic toxicity to drug administered*** - **Lip numbness** and apprehension immediately following epidural lidocaine injection are classic signs of **local anesthetic systemic toxicity (LAST)** due to unintended intravascular injection. - The rapid onset of symptoms suggests direct access to the systemic circulation via a blood vessel, leading to high plasma concentrations of lidocaine. *Allergy to drug administered* - Allergic reactions to local anesthetics are rare and typically involve **urticaria**, **bronchospasm**, or **anaphylaxis**, which are not described here. - Symptoms of allergy usually do not include lip numbness and apprehension as the primary manifestations. *Vasovagal shock* - Vasovagal reactions are characterized by **bradycardia**, **hypotension**, and syncope, usually triggered by pain or anxiety. - While apprehension is present, the specific symptom of lip numbness is not typical of a vasovagal response. *Drug entered SA space* - If the drug had entered the subarachnoid (SA) space, the patient would likely experience a **rapid onset of profound motor and sensory block**, potentially leading to **total spinal anesthesia** and respiratory compromise. - Lip numbness and apprehension are not primary indicators of inadvertent subarachnoid injection; rather, they point to systemic absorption.
Question 8: Which intravenous anaesthetic agent has analgesic effect also
- A. Thiopentone
- B. Ketamine (Correct Answer)
- C. Propofol
- D. Etomidate
Explanation: ***Ketamine*** - Ketamine acts as an **N-methyl-D-aspartate (NMDA) receptor antagonist**, providing significant **analgesia** in addition to its anaesthetic effects. - It induces a state of **dissociative anaesthesia**, where the patient appears awake but is unresponsive to pain, making it unique among intravenous anaesthetics. *Thiopentone* - Thiopentone is a **barbiturate** that acts as a potent hypnotic and anaesthetic but provides no significant analgesic properties. - It can even cause **anti-analgesia** (hyperalgesia) at sub-hypnotic doses, increasing sensitivity to pain. *Propofol* - Propofol is a potent intravenous anaesthetic that works primarily as a **GABA-A receptor agonist**, but it lacks intrinsic analgesic properties. - While it can cause some sedation and reduced pain perception due to CNS depression, it does not directly modulate pain pathways in the way an analgesic would. *Etomidate* - Etomidate is a hypnotic agent highly valued for its **cardiovascular stability**, making it suitable for patients with compromised cardiac function. - Like propofol and thiopentone, etomidate primarily acts on **GABA-A receptors** to induce unconsciousness and offers no significant analgesic effects.
Question 9: A patient undergoing a minor surgical procedure is given lignocaine injection. Assertion: Local anaesthetics act by blocking nerve conduction. Reason: Small fibers and non-myelinated fibers are blocked more easily than large myelinated fibers.
- A. Assertion is false, but Reason is true
- B. Both Assertion and Reason are true, and Reason is not the correct explanation for Assertion (Correct Answer)
- C. Both Assertion and Reason are true, and Reason is the correct explanation for Assertion
- D. Assertion is true, but Reason is false
Explanation: ***Both Assertion and Reason are true, and Reason is NOT the correct explanation for Assertion*** - The **Assertion** is true: Local anesthetics (like lignocaine) block nerve conduction by inhibiting **voltage-gated sodium channels**, preventing the depolarization necessary for action potential propagation - The **Reason** is also true: Small diameter and non-myelinated fibers (like C and Aδ pain fibers) are blocked more easily than large myelinated fibers (like Aα motor fibers), which explains the **differential blockade** pattern seen clinically - However, the **Reason does NOT explain WHY** local anesthetics block nerve conduction—it describes **WHICH** nerve fibers are blocked preferentially. The mechanism of blocking conduction is sodium channel inhibition, not fiber size selectivity - The differential sensitivity is a consequence of fiber characteristics (surface area-to-volume ratio, number of nodes of Ranvier), not the explanation for the blocking mechanism itself *Both Assertion and Reason are true, and Reason is the correct explanation for Assertion* - While both statements are individually true, the Reason does not explain the **mechanism** by which local anesthetics block nerve conduction - The Reason addresses fiber **selectivity**, which is a separate pharmacological property from the **mechanism of action** (sodium channel blockade) *Assertion is true, but Reason is false* - The Assertion is demonstrably true—local anesthetics block nerve conduction - The Reason is also true—this is well-established pharmacology: autonomic (small) > sensory (medium) > motor (large) fiber blockade sequence *Assertion is false, but Reason is true* - The Assertion is fundamentally correct and represents the primary pharmacological action of local anesthetics - Blocking nerve conduction is the therapeutic goal of local anesthetic administration
Question 10: Which is correct about the anesthetic drugs X and Y in the image shown? (Recent NEET Pattern 2016-17)
- A. Drug X and Y have equally fast onset of action
- B. Drug X and Y have equally fast onset of action but potency of X is more than Y
- C. Drug Y is more fast acting than X
- D. Drug X is more fast acting than Y (Correct Answer)
Explanation: ***Drug X is more fast acting than Y*** - The **oil:gas partition coefficient** for Drug X is lower than for Drug Y. A lower oil:gas partition coefficient typically correlates with a **faster onset of action** for inhaled anesthetics as it indicates lower solubility in blood and tissues, allowing for quicker equilibration in the brain. - While MAC is plotted against oil:gas partition coefficient, the question specifically asks about **onset of action**, which is primarily influenced by blood-gas solubility rather than oil-gas solubility. However, an anesthetic with lower oil-gas solubility (like X) would generally also have lower blood-gas solubility, leading to faster onset. *Drug Y is more fast acting than X* - Drug Y has a **higher oil:gas partition coefficient** compared to Drug X, indicating greater lipid solubility. - A higher oil:gas partition coefficient generally correlates with a **slower onset of action** for inhaled anesthetics, as more drug dissolves in lipids before reaching the brain. *Drug X and Y have equally fast onset of action* - The graph clearly shows that Drug X and Drug Y have different **oil:gas partition coefficients**. - Since the partition coefficients are different, their **solubility characteristics** and therefore their clinical onset of action would also be different. *Drug X and Y have equally fast onset of action but potency of X is more than Y* - Onset of action is **not equal** for X and Y due to their differing oil:gas partition coefficients. - Potency, represented by **MAC** (Minimum Alveolar Concentration), is inversely related to the oil:gas partition coefficient for many inhaled anesthetics. From the graph, Drug X has a higher MAC value than Drug Y (meaning it is **less potent** but acts faster).
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