General Anesthesia — MCQs

General Anesthesia Indian Medical PG Practice Questions and MCQs

Question 301: Which muscle relaxant can be safely administered in patients with renal disease?

A. Doxacurium
B. Pancuronium
C. Vecuronium (Correct Answer)
D. Gallamine

Explanation: **Explanation:** The choice of muscle relaxant in renal disease depends on the drug's route of elimination. In patients with renal failure, drugs primarily excreted by the kidneys will have a prolonged duration of action and increased risk of toxicity. **Why Vecuronium is the correct answer:** Vecuronium is an intermediate-acting aminosteroid neuromuscular blocker. It is primarily metabolized by the **liver** and excreted via **bile** (approx. 40-50%), with only about 20-30% excreted unchanged in the urine. While its duration may be slightly prolonged in severe renal failure due to its active metabolite (3-desacetyl vecuronium), it is considered significantly safer than long-acting agents. *Note: While Atracurium and Cisatracurium (via Hoffman elimination) are the "gold standard" for renal failure, among the given options, Vecuronium is the safest choice.* **Analysis of Incorrect Options:** * **A. Doxacurium:** A long-acting benzylisoquinolinium that is primarily eliminated by the kidneys. It is contraindicated or used with extreme caution in renal failure. * **B. Pancuronium:** A long-acting agent where approximately 80% is excreted unchanged in the urine. It causes significant "recurarization" in renal patients. * **D. Gallamine:** This drug is **100% excreted by the kidneys**. It is absolutely contraindicated in renal failure as it will not be cleared from the body. **NEET-PG High-Yield Pearls:** * **Drug of Choice for Renal/Hepatic Failure:** **Cisatracurium** (preferred over Atracurium as it does not cause histamine release). * **Hoffman Elimination:** A non-enzymatic, pH and temperature-dependent degradation (used by Atracurium/Cisatracurium). * **Mivacurium:** Metabolized by plasma cholinesterase (like Succinylcholine). * **Rocunorium:** Primarily eliminated by the liver; useful for rapid sequence induction when Succinylcholine is contraindicated.

Question 302: Phase II block is seen in which of the following?

A. Suxamethonium (Sch) (Correct Answer)
B. d-Tubocurarine (d-TC)
C. Ether
D. Nitrous Oxide (N2O)

Explanation: **Explanation:** **Phase II Block** (also known as Dual Block or Desensitization Block) is a characteristic phenomenon associated with **Suxamethonium (Succinylcholine)**, a depolarizing neuromuscular blocker. 1. **Why Suxamethonium is correct:** Normally, Suxamethonium produces a **Phase I block** (depolarizing block) characterized by fasciculations followed by paralysis. However, when administered in **large doses, repeated boluses, or via continuous infusion**, the post-junctional membrane becomes desensitized. Even though the membrane repolarizes, it becomes insensitive to Acetylcholine. At this stage, the block changes its characteristics to resemble a non-depolarizing block (showing "fade" on Train-of-Four monitoring and post-tetanic facilitation). This transition is the Phase II block. 2. **Why other options are incorrect:** * **d-Tubocurarine (d-TC):** This is a classic non-depolarizing neuromuscular blocker. It produces a competitive block from the onset; it does not transition through phases. * **Ether:** An inhalational anesthetic that can potentiate neuromuscular blockade but does not cause a Phase II block itself. * **Nitrous Oxide (N2O):** An inhalational gas with minimal effect on the neuromuscular junction. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** Phase II block is identified using a Peripheral Nerve Stimulator; it shows **Fade** in Train-of-Four (TOF) stimulation. * **Reversal:** Unlike Phase I block (where Neostigmine worsens the block), a Phase II block can potentially be reversed with **Anticholinesterases (Neostigmine)**, though this must be done cautiously with nerve stimulator guidance. * **Risk Factor:** Patients with **Pseudocholinesterase deficiency** are at high risk of developing Phase II block even with standard doses of Suxamethonium due to prolonged exposure at the NMJ.

Question 303: Which of the following intravenous induction agents suppresses steroidogenesis?

A. Thiopentone
B. Propofol
C. Ketamine
D. Etomidate (Correct Answer)

Explanation: **Explanation:** **Etomidate** is the correct answer because it is a potent, dose-dependent inhibitor of the enzyme **11-beta-hydroxylase**. This enzyme is essential for the conversion of 11-deoxycortisol to cortisol and 11-deoxycorticosterone to aldosterone in the adrenal cortex. Even a single induction dose of etomidate can suppress adrenal steroidogenesis for 6 to 24 hours, potentially leading to secondary adrenal insufficiency. While this makes it less ideal for long-term sedation in the ICU, it remains a popular choice for induction in hemodynamically unstable patients due to its minimal cardiovascular effects. **Analysis of Incorrect Options:** * **Thiopentone (A):** A barbiturate that acts on GABA-A receptors. Its primary side effects are cardiovascular depression and histamine release; it does not affect the adrenal axis. * **Propofol (B):** The most common induction agent. It causes significant vasodilation and hypotension but has no inhibitory effect on steroid synthesis. * **Ketamine (C):** A dissociative anesthetic that acts as an NMDA receptor antagonist. It actually *stimulates* the sympathetic nervous system, increasing heart rate and blood pressure, rather than suppressing hormonal pathways. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Etomidate is the drug of choice for induction in patients with **cardiovascular disease, shock, or hypovolemia** because it maintains hemodynamic stability. * **Myoclonus:** Etomidate is frequently associated with involuntary muscle movements (myoclonus) during induction. * **Porphyria:** Etomidate (like Thiopentone) should be avoided in patients with acute intermittent porphyria as it can induce the enzyme ALA synthase. * **Key Enzyme:** Always remember **11-beta-hydroxylase** as the specific target for etomidate-induced adrenal suppression.

Question 304: Regarding suxamethonium, all are true except?

A. It is metabolized principally by plasma cholinesterase.
B. It should be used cautiously in patients using echothiopate eye drops for glaucoma.
C. It is recommended in patients with burns. (Correct Answer)
D. It can cause hyperkalemia.

Explanation: **Explanation:** Suxamethonium (Succinylcholine) is a depolarizing neuromuscular blocker. The correct answer is **C** because suxamethonium is strictly **contraindicated** in patients with major burns. **1. Why Option C is the correct answer (The Exception):** In patients with extensive burns (typically after 24–48 hours), there is an **upregulation of extrajunctional acetylcholine receptors** (immature $\alpha$7 receptors) across the muscle membrane. When suxamethonium binds to these receptors, it causes prolonged depolarization and a massive efflux of potassium from the cells. This can lead to **severe hyperkalemia**, resulting in cardiac arrhythmias or cardiac arrest. **2. Analysis of other options:** * **Option A:** Suxamethonium has a very short duration of action because it is rapidly hydrolyzed by **plasma cholinesterase** (pseudocholinesterase), not by acetylcholinesterase at the NMJ. * **Option B:** Echothiopate is an irreversible cholinesterase inhibitor used for glaucoma. It depletes plasma cholinesterase levels, thereby significantly **prolonging the duration of action** of suxamethonium (causing prolonged apnea). * **Option D:** In healthy individuals, suxamethonium causes a transient, mild rise in serum potassium (approx. 0.5 mEq/L). However, in specific pathological states, this rise is exaggerated. **Clinical Pearls for NEET-PG:** * **Drug of Choice:** For **Rapid Sequence Induction (RSI)** due to its rapid onset (30–60s) and short duration (5–10 mins). * **Contraindications:** Burns, massive trauma, upper/lower motor neuron lesions (paralysis), and a personal/family history of **Malignant Hyperthermia**. * **Side Effects:** Muscle fasciculations (prevented by a "pre-curarization" dose), myalgia, increased intraocular/intragastric pressure, and bradycardia (especially in children or upon second dose).

Question 305: Which of the following is an epileptogenic anesthetic agent?

A. Isoflurane
B. Sevoflurane (Correct Answer)
C. Methoxyflurane
D. Halothane

Explanation: **Explanation:** **Sevoflurane (Option B)** is the correct answer because it is uniquely associated with **epileptiform EEG activity** (spikes and waves) and occasional clinical seizure-like movements, even in patients without a history of epilepsy. This pro-convulsant effect is most commonly observed during **deep anesthesia** (high concentrations) and when the patient is **hypocapnic** (due to hyperventilation). Despite this, it remains the agent of choice for inhalational induction due to its non-pungency. **Analysis of Incorrect Options:** * **Isoflurane (Option A):** It is considered **neuroprotective**. It suppresses metabolic rate and EEG activity in a dose-dependent manner, eventually leading to burst suppression. It does not trigger seizures. * **Methoxyflurane (Option C):** Primarily known for its **nephrotoxicity** (due to inorganic fluoride release). It does not have significant epileptogenic properties. * **Halothane (Option D):** While it can sensitize the myocardium to catecholamines (arrhythmogenic), it is not associated with seizure activity. **High-Yield Clinical Pearls for NEET-PG:** * **Epileptogenic Anesthetics:** Apart from Sevoflurane, other agents to remember are **Enflurane** (classic association with seizures), **Ketamine**, and **Etomidate** (can trigger myoclonus and is used to map seizure foci). * **Drug of Choice for Epilepsy:** **Thiopentone** is the gold standard for brain protection and seizure suppression. **Propofol** also has potent anticonvulsant properties (though it may rarely cause non-epileptic myoclonus). * **Methoxyflurane** is the most potent inhalational agent (lowest MAC) but is obsolete due to "high-output renal failure."

Question 306: Which of the following is NOT an intravenous anesthetic agent?

A. Ketamine
B. Thiopentone
C. Etomidate
D. Cyclopropane (Correct Answer)

Explanation: **Explanation:** The classification of general anesthetics is a high-yield topic for NEET-PG. Anesthetic agents are primarily divided into two categories based on their route of administration: **Intravenous (IV)** and **Inhalational**. **Why Cyclopropane is the Correct Answer:** **Cyclopropane** is a potent **inhalational anesthetic** (gas). While historically significant for its rapid induction and maintenance of cardiac output, it is no longer used in modern clinical practice because it is highly **explosive and flammable**. It also sensitizes the myocardium to catecholamines, increasing the risk of arrhythmias. **Analysis of Incorrect Options (IV Anesthetics):** * **Ketamine:** A phencyclidine derivative used intravenously to produce "dissociative anesthesia." It is unique because it provides profound analgesia and stimulates the sympathetic nervous system. * **Thiopentone:** A short-acting barbiturate that was previously the "gold standard" for IV induction. It acts via GABA-A receptors but has been largely replaced by Propofol. * **Etomidate:** An IV induction agent favored for hemodynamically unstable patients (e.g., trauma or heart failure) because it causes minimal cardiovascular and respiratory depression. **Clinical Pearls for NEET-PG:** * **Etomidate Side Effect:** Known for causing transient **adrenocortical suppression** by inhibiting the enzyme 11-beta-hydroxylase. * **Ketamine Clinical Use:** The drug of choice for induction in patients with **bronchial asthma** (due to bronchodilation) and **hypovolemic shock**. * **Inhalational Agents:** Other common examples include Halothane, Isoflurane, Sevoflurane, and Desflurane. * **Thiopentone:** Associated with a garlic/onion taste sensation during induction and can trigger laryngeal spasms.

Question 307: Which of the following intravenous anesthetic agents suppresses cortisol synthesis?

A. Propofol
B. Ketamine
C. Etomidate (Correct Answer)
D. Thiopentone

Explanation: **Explanation:** The correct answer is **Etomidate**. **Why Etomidate is correct:** Etomidate is a carboxylated imidazole derivative used for the induction of anesthesia. Its most significant side effect is the **dose-dependent inhibition of the enzyme 11-beta-hydroxylase**. This enzyme is essential for the conversion of 11-deoxycortisol to cortisol in the adrenal cortex. Even a single induction dose can suppress cortisol and aldosterone synthesis for 6 to 24 hours, which may lead to secondary adrenal insufficiency. This makes it a poor choice for patients with sepsis or those requiring long-term sedation in the ICU. **Why the other options are incorrect:** * **Propofol:** An isopropylphenol that acts via GABA-A receptors. It does not interfere with steroidogenesis; its primary side effects are hypotension and respiratory depression. * **Ketamine:** A NMDA receptor antagonist. It actually stimulates the sympathetic nervous system, leading to an increase in heart rate and blood pressure, rather than suppressing adrenal function. * **Thiopentone:** An ultra-short-acting barbiturate. While it causes cardiovascular and respiratory depression, it has no specific inhibitory effect on adrenal enzymes. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Etomidate is the induction agent of choice for **hemodynamically unstable patients** (e.g., trauma, severe valvular heart disease) because it has minimal effects on heart rate and blood pressure. * **Myoclonus:** Etomidate is frequently associated with excitatory movements (myoclonus) during induction, which can be prevented by pre-medication with opioids or benzodiazepines. * **Porphyria:** Etomidate is contraindicated in patients with porphyria as it can induce the enzyme ALA synthetase.

Question 308: Which side effect of halothane is countered by atropine?

A. Bradycardia (Correct Answer)
B. Hypotension
C. Hyperthermia
D. Constipation

Explanation: **Explanation:** **Halothane** is a potent volatile anesthetic known for its significant effects on the cardiovascular system. The correct answer is **Bradycardia** because halothane increases vagal (parasympathetic) tone and has a direct depressant effect on the sinoatrial (SA) node. **Atropine**, an anticholinergic/antimuscarinic agent, blocks the action of the vagus nerve on the heart, thereby increasing the heart rate and effectively countering halothane-induced bradycardia. **Analysis of Incorrect Options:** * **B. Hypotension:** While halothane causes hypotension (primarily via direct myocardial depression and reduced cardiac output), atropine is not the primary treatment. Hypotension is managed by reducing anesthetic depth or administering vasopressors/fluids. * **C. Hyperthermia:** Halothane is a known trigger for **Malignant Hyperthermia**. Atropine has no role in treating this; the definitive treatment is **Dantrolene**. In fact, atropine can worsen hyperthermia by inhibiting sweating. * **D. Constipation:** While anticholinergics like atropine cause constipation, this is not a side effect of halothane, nor is it a clinical concern managed in the acute anesthetic setting. **High-Yield Clinical Pearls for NEET-PG:** * **Halothane Hepatitis:** A rare but serious immune-mediated hepatotoxicity (more common in adults/obese patients). * **Catecholamine Sensitivity:** Halothane sensitizes the myocardium to endogenous and exogenous catecholamines (epinephrine), increasing the risk of ventricular arrhythmias. * **"Halothane Shakes":** Post-operative shivering is common with halothane. * **Uterine Relaxation:** Halothane causes significant uterine smooth muscle relaxation, which can lead to postpartum hemorrhage if used in obstetrics.

Question 309: Which anesthetic agent is least metabolized in the body?

A. Xenon (Correct Answer)
B. Ether
C. Halothane
D. Methoxyflurane

Explanation: **Explanation:** The degree of metabolism of an anesthetic agent is a critical factor in determining its toxicity and duration of action. **Correct Option: A. Xenon** Xenon is a noble gas and is considered the "ideal" anesthetic. It is chemically inert and does not undergo any biotransformation or metabolism in the human body (0% metabolism). It is eliminated entirely unchanged via the lungs. This lack of metabolism makes it non-toxic to the liver and kidneys. **Incorrect Options:** * **B. Ether:** Diethyl ether undergoes approximately 2–5% hepatic metabolism. While relatively low, it is significantly higher than Xenon. * **C. Halothane:** Halothane is highly metabolized in the liver (up to 15–20%). Its metabolites (trifluoroacetic acid) are associated with "Halothane Hepatitis," a rare but severe immune-mediated liver injury. * **D. Methoxyflurane:** This agent has the highest rate of metabolism among volatile anesthetics (approx. 50–70%). Its metabolism releases inorganic fluoride ions, which are highly nephrotoxic, leading to its withdrawal from routine clinical use. **High-Yield NEET-PG Pearls:** * **Metabolism Hierarchy (Highest to Lowest):** Methoxyflurane (50-70%) > Halothane (15-20%) > Enflurane (2%) > Sevoflurane (2-5%) > Isoflurane (0.2%) > Desflurane (0.02%) > **Xenon (0%)**. * **Xenon Properties:** It has a very low blood-gas partition coefficient (0.115), leading to extremely rapid induction and recovery. It is also cardioprotective and neuroprotective. * **Clinical Constraint:** Despite being ideal, Xenon is not widely used because it is expensive to extract and requires specialized closed-circuit delivery systems.

Question 310: What effect does ketamine produce?

A. Analgesia (Correct Answer)
B. Allodynia
C. Hyperpathia
D. Dystonia

Explanation: **Explanation:** **Ketamine** is a unique induction agent known for producing **dissociative anesthesia**. It acts primarily as a non-competitive antagonist at the **NMDA (N-methyl-D-aspartate) receptors** in the brain and spinal cord. 1. **Why Analgesia is correct:** Ketamine is a potent **analgesic**, even at sub-anesthetic doses. By inhibiting NMDA receptors, it blocks the transmission of pain signals in the dorsal horn of the spinal cord. It is particularly effective for somatic pain and is often used in "multimodal analgesia" to reduce opioid requirements and prevent opioid-induced hyperalgesia. 2. **Why the other options are incorrect:** * **Allodynia:** This refers to pain resulting from a stimulus that does not normally provoke pain (e.g., a light touch). Ketamine is used to *treat* neuropathic pain conditions involving allodynia, rather than causing it. * **Hyperpathia:** This is an exaggerated or delayed pain response to a repetitive stimulus. Like allodynia, this is a symptom of nerve damage that ketamine helps alleviate. * **Dystonia:** This refers to involuntary muscle contractions. While ketamine can cause "catalepsy" (muscle rigidity and fixed posture), it is not typically associated with clinical dystonia. **High-Yield Clinical Pearls for NEET-PG:** * **Dissociative State:** Characterized by eyes remaining open with a slow nystagmic gaze (disconnected but not asleep). * **Sympathomimetic Effect:** Unlike most induction agents, ketamine **increases** HR, BP, and CO (Drug of choice for **hypovolemic shock**). * **Airway:** It maintains airway reflexes and causes **bronchodilation** (Drug of choice for **asthmatic patients**). * **Adverse Effect:** **Emergence delirium/hallucinations** (minimized by co-administration of benzodiazepines like Midazolam). * **Contraindication:** Historically avoided in patients with increased intracranial pressure (ICP) and intraocular pressure (IOP).

Practice by Chapter

History of Anesthesia

Practice Questions

Preoperative Evaluation

Practice Questions

Pharmacology of Inhalational Anesthetics

Practice Questions

Pharmacology of Intravenous Anesthetics

Practice Questions

Neuromuscular Blocking Agents

Practice Questions

Airway Management

Practice Questions

Endotracheal Intubation

Practice Questions

Difficult Airway Algorithms

Practice Questions

Intraoperative Monitoring

Practice Questions

Depth of Anesthesia Monitoring

Practice Questions

Emergence from Anesthesia

Practice Questions

Postoperative Care

Practice Questions

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