NEET-PG 2013 — Anesthesiology
33 Previous Year Questions with Answers & Explanations
Ether was first used as an anesthetic by?
Phase II block is seen with:
What is the drug of choice for reversing muscle relaxants after anesthesia?
What is the primary clinical use of Sugammadex in anesthesia?
Which anaesthetic agent has maximum MAC ?
In which vein is Central Venous Pressure (CVP) most accurately monitored?
Central venous monitoring is typically used for all of the following except:
Which of the following statements about Nitrous Oxide (N2O) is true?
Dissociative anaesthesia is produced by?
Which of the following anesthetic agents causes the LEAST severe complications when accidentally injected intra-arterially?
NEET-PG 2013 - Anesthesiology NEET-PG Practice Questions and MCQs
Question 1: Ether was first used as an anesthetic by?
- A. Morton (Correct Answer)
- B. Wells
- C. Simpson
- D. Priestly
Explanation: ***Morton*** - **William T.G. Morton**, a dentist, publicly demonstrated the use of **ether as a surgical anesthetic** in 1846 during a tooth extraction at Massachusetts General Hospital. - This event marked a pivotal moment in medicine, revolutionizing surgical practices by providing effective pain relief. *Priestly* - **Joseph Priestley** was an 18th-century chemist who discovered several gases, including **oxygen**, but was not involved in the anesthetic use of ether. - His work was foundational to understanding the composition of air but did not extend to surgical applications of inhaled substances. *Wells* - **Horace Wells**, an American dentist, was an early pioneer in anesthesia who experimented with **nitrous oxide** as an anesthetic for tooth extractions. - While significant, his work predated and differed from Morton's successful public demonstration and widespread adoption of ether. *Simpson* - **James Young Simpson**, a Scottish obstetrician, is credited with pioneering the use of **chloroform** as an anesthetic, particularly in childbirth. - His contributions were later than Morton's use of ether and involved a different anesthetic agent.
Question 2: Phase II block is seen with:
- A. SCh infusion (Correct Answer)
- B. Single dose SCh
- C. Mivacurium
- D. None of the options
Explanation: ***SCh infusion*** - A **prolonged infusion or high dose** of succinylcholine (SCh) can lead to a **Phase II block**, a desensitizing block resembling that of a non-depolarizing neuromuscular blocker. - This occurs due to the **persistent presence of SCh** at the neuromuscular junction, which initially depolarizes the endplate (Phase I) but eventually leads to **receptor desensitization** and repolarization, preventing further muscle contraction. *Single dose SCh* - A **single bolus dose of succinylcholine** typically produces a **Phase I block**, characterized by initial muscle fasciculations followed by flaccid paralysis due to persistent depolarization of the motor endplate. - It resolves relatively quickly as **succinylcholine is rapidly hydrolyzed** by pseudocholinesterase, usually not leading to a prolonged desensitization characteristic of Phase II. *Mivacurium* - **Mivacurium** is an intermediate-acting, **non-depolarizing neuromuscular blocker**. - Its mechanism of action involves **competitively binding to nicotinic acetylcholine receptors** at the neuromuscular junction, thereby preventing acetylcholine from binding and initiating muscle contraction, which is fundamentally different from a Phase II block caused by prolonged depolarization. *None of the options* - This option is incorrect because **SCh infusion** is a recognized cause of Phase II block. - The phenomenon of Phase II block is a well-established pharmacological response to **excessive and prolonged exposure** to depolarizing neuromuscular blockers like succinylcholine.
Question 3: What is the drug of choice for reversing muscle relaxants after anesthesia?
- A. Pralidoxine
- B. Neostigmine (Correct Answer)
- C. Atropine
- D. None of the options
Explanation: ***Neostigmine*** - **Neostigmine** is an **acetylcholinesterase inhibitor** that increases the amount of acetylcholine at the neuromuscular junction, thereby reversing the effects of non-depolarizing muscle relaxants. - It is often co-administered with an **anticholinergic agent** like atropine or glycopyrrolate to counteract its muscarinic side effects (e.g., bradycardia, increased secretions). *Pralidoxine* - **Pralidoxine (2-PAM)** is an **oxime cholinesterase reactivator** used primarily to treat organophosphate poisoning. - It works by regenerating acetylcholinesterase that has been inhibited by organophosphates, which is not the mechanism of action required for reversing typical muscle relaxants. *Atropine* - **Atropine** is an **anticholinergic drug** that blocks muscarinic acetylcholine receptors. - While it is often given with neostigmine to counteract muscarinic side effects like bradycardia, it does not directly reverse the neuromuscular blockade caused by muscle relaxants. *None of the options* - This option is incorrect because **neostigmine** is a well-established and commonly used drug for reversing non-depolarizing muscle relaxants.
Question 4: What is the primary clinical use of Sugammadex in anesthesia?
- A. Organophosphate poisoning
- B. Reversal of NM blockers (Correct Answer)
- C. Treatment of local anaesthetic poisoning
- D. Treatment of central anticholinergic syndrome
Explanation: ***Reversal of NM blockers*** - **Sugammadex** is a modified gamma-cyclodextrin that specifically encapsulates steroidal **neuromuscular blocking agents (NMBAs)** like **rocuronium** and **vecuronium**. - This encapsulation rapidly inactivates the NMBAs, leading to a dose-dependent and swift **reversal of neuromuscular blockade**. *Organophosphate poisoning* - Organophosphate poisoning is treated with **atropine** to block muscarinic effects and **pralidoxime** to reactivate inhibited acetylcholinesterase. - Sugammadex has no role in antagonizing the effects of **organophosphates** or regenerating acetylcholinesterase. *Treatment of local anaesthetic poisoning* - Local anesthetic systemic toxicity (LAST) is primarily managed with supportive care, including airway management, and the administration of **lipid emulsion therapy**. - Sugammadex does not bind to local anesthetics and therefore has no efficacy in treating local anesthetic poisoning. *Treatment of central anticholinergic syndrome* - Central anticholinergic syndrome is typically treated with **physostigmine**, an acetylcholinesterase inhibitor that can cross the blood-brain barrier. - Sugammadex is not an anticholinergic antagonist and does not affect the central nervous system to reverse anticholinergic effects.
Question 5: Which anaesthetic agent has maximum MAC ?
- A. Ether
- B. Methoxyfluorane
- C. Halothane
- D. Nitrous Oxide (N2O) (Correct Answer)
Explanation: ***Nitrous Oxide (N2O)*** - **Nitrous Oxide** has the highest **minimum alveolar concentration (MAC)** of all commonly used inhalational anesthetics, approximately 104%. - A high MAC indicates **low potency**, meaning that a large concentration is required to achieve anesthetic effects. *Ether* - **Ether** has a MAC of about 1.92%, which is significantly lower than that of Nitrous Oxide. - Its use has largely been replaced due to its flammability, slow induction, and recovery times. *Methoxyfluorane* - **Methoxyfluorane** is known for having a very low MAC, around 0.16%, making it the most potent inhalational anesthetic. - Due to its high potency and significant nephrotoxicity, its use is now very limited. *Halothane* - **Halothane** has a MAC of approximately 0.75%. - While it was a widely used inhalational anesthetic, it has largely been replaced due to concerns about **halothane hepatitis** and arrhythmogenicity.
Question 6: In which vein is Central Venous Pressure (CVP) most accurately monitored?
- A. Anterior jugular vein
- B. External jugular vein
- C. Inferior vena cava
- D. Internal jugular vein (Correct Answer)
Explanation: ***Internal jugular vein*** - The **internal jugular vein** provides the **most direct and consistent access** to the superior vena cava and right atrium, where CVP is accurately measured. - Its straight course and reliable anatomical landmarks make it a preferred site for CVP catheter insertion. *Anterior jugular vein* - The **anterior jugular vein** is smaller and often has a more tortuous course, making consistent and reliable CVP monitoring difficult. - It is not typically chosen for central venous access due to its anatomical variability and smaller caliber. *External jugular vein* - The **external jugular vein** is superficially located and easier to access but often has valves and a more oblique angle to the subclavian vein, making catheter advancement to the central circulation challenging. - Catheter tip placement is less consistent for accurate CVP measurements compared to the internal jugular vein. *Inferior vena cava* - While the **inferior vena cava** eventually drains into the right atrium, access is typically via the femoral vein, which is associated with a higher risk of infection and deep vein thrombosis for long-term CVP monitoring. - Measurements from the inferior vena cava or femoral vein can be affected by **intra-abdominal pressure** and are not as accurately reflective of right atrial pressure as those from the superior vena cava.
Question 7: Central venous monitoring is typically used for all of the following except:
- A. Administering thrombolytics (Correct Answer)
- B. Deciding the need for plasma infusion
- C. Deciding the requirement for blood transfusion
- D. Regulating the speed and amount of fluid infusion
Explanation: ***Administering thrombolytics*** - Central venous monitoring is a technique used to measure central venous pressure (CVP), which reflects right atrial pressure and indirectly **right ventricular preload**. It does not directly relate to the administration of **thrombolytics**. - Thrombolytics are typically administered intravenously through a peripheral or central line to dissolve clots, but CVP monitoring is not a prerequisite or a direct function of this administration. *Regulating the speed and amount of fluid infusion* - **Central venous pressure (CVP)** monitoring is crucial for assessing a patient's **fluid status** and guiding fluid resuscitation. - By continuously monitoring CVP, clinicians can determine whether to increase, decrease, or maintain the rate of **fluid infusion** to optimize cardiac preload without causing fluid overload. *Deciding the need for plasma infusion* - CVP values help assess **circulatory volume** and guide decisions on fluid replacement, including the need for **plasma infusion** in conditions like severe hypovolemia or coagulopathy. - A low CVP in a patient with bleeding or coagulation issues might indicate the need for volume expansion with **plasma**. *Deciding the requirement for blood transfusion* - **Low CVP** can indicate **hypovolemia**, which might be due to blood loss, thereby suggesting the need for a **blood transfusion**. - While not the sole determinant, CVP is one of several physiological parameters used to assess the urgency and amount of **blood products** required to restore circulating volume and oxygen-carrying capacity.
Question 8: Which of the following statements about Nitrous Oxide (N2O) is true?
- A. Least potent inhalational anesthetic (Correct Answer)
- B. Lighter than air
- C. Effective muscle relaxant
- D. Does not cause diffusion hypoxia
Explanation: **Least potent inhalational anesthetic** - Nitrous oxide has a **high Minimum Alveolar Concentration (MAC)** of approximately 104%, making it the least potent of the commonly used inhalational anesthetics. - Its high MAC means a very high concentration is required to achieve surgical anesthesia, which is why it is typically used as an adjunct to more potent agents. *Lighter than air* - The molecular weight of nitrous oxide (N2O) is 44, which is **heavier than air** (average molecular weight approximately 29 g/mol). - Its density is greater than air, meaning it would tend to sink rather than rise. *Effective muscle relaxant* - Nitrous oxide provides **minimal to no skeletal muscle relaxation** benefits. - If muscle relaxation is required, a neuromuscular blocking agent must be administered separately. *Does not cause diffusion hypoxia* - Nitrous oxide rapidly diffuses out of the blood into the alveoli during emergence, diluting the oxygen and carbon dioxide there. - This rapid diffusion can lead to **diffusion hypoxia** (also known as the "second gas effect"), necessitating the administration of 100% oxygen during recovery to prevent this complication.
Question 9: Dissociative anaesthesia is produced by?
- A. Ketamine (Correct Answer)
- B. Etomidate
- C. Propofol
- D. Thiopentone
Explanation: ***Ketamine*** - **Ketamine** is a unique anesthetic that produces a state of **dissociative anesthesia**, characterized by a trance-like state, analgesia, amnesia, and catalepsy. - This effect is primarily due to its antagonism of the **N-methyl-D-aspartate (NMDA) receptor**. *Etomidate* - **Etomidate** is an intravenous anesthetic characterized by its **cardiovascular stability**, making it suitable for patients with heart conditions. - It works primarily by modulating **GABA-A receptors** but does not produce dissociative anesthesia. *Propofol* - **Propofol** is a widely used intravenous anesthetic known for its **rapid onset and recovery**, and it is often used for induction and maintenance of general anesthesia. - Its primary mechanism of action involves enhancing the effects of **GABA-A receptors**, leading to central nervous system depression, but not dissociative anesthesia. *Thiopentone* - **Thiopentone** (Thiopental) is a barbiturate anesthetic that causes rapid loss of consciousness and has been historically used for inducing general anesthesia. - It acts as a **GABA-A receptor agonist**, depressing the central nervous system, but it does not produce the distinct dissociative state seen with ketamine.
Question 10: Which of the following anesthetic agents causes the LEAST severe complications when accidentally injected intra-arterially?
- A. Thiopentone
- B. Propofol (Correct Answer)
- C. Methohexitone
- D. Midazolam
Explanation: **Propofol** * **Propofol** has a relatively low incidence and severity of complications if accidentally injected intra-arterially because of its **lipid emulsion formulation** and mild irritant properties compared to other agents. * While any intra-arterial injection can cause problems, the milder venoconstriction and less direct tissue damage make its intra-arterial complication profile less severe than alternative agents. *Thiopentone* * **Thiopentone** (Thiopental) is highly alkaline, and accidental intra-arterial injection can cause **intense pain**, **vasospasm**, and **gangrene** due to precipitation in the arterioles and widespread endothelial damage. * This severe complication arises from its extreme pH and crystal formation, leading to profound ischemia. *Midazolam* * Accidental intra-arterial injection of **Midazolam** can cause **pain**, **spasm**, and **local tissue damage** due to its relatively acidic pH and solvent properties, though generally less severe than thiopentone. * While not as catastrophic as thiopentone, it can still lead to significant discomfort and localized vascular issues. *Methohexitone* * **Methohexitone** is also an alkaline barbiturate derivative, similar in nature to thiopentone, and its intra-arterial injection carries a significant risk of **vasospasm**, **pain**, and potentially **tissue necrosis**. * Its strong irritant properties and ability to precipitate within the vasculature make it a dangerous agent for inadvertent intra-arterial administration.