General Anesthesia — MCQs

General Anesthesia Indian Medical PG Practice Questions and MCQs

Question 291: Which of the following is NOT an action of depolarizing agents?

A. Bradycardia
B. Hypokalemia (Correct Answer)
C. Increased intracranial tension
D. Increased intraocular pressure

Explanation: **Explanation:** The correct answer is **B. Hypokalemia**. Depolarizing neuromuscular blocking agents, specifically **Succinylcholine (Suxamethonium)**, are known to cause **Hyperkalemia**, not hypokalemia. **1. Why Hypokalemia is the correct answer (The Mechanism):** Succinylcholine acts by mimicking acetylcholine at the nicotinic receptors of the neuromuscular junction. It causes prolonged depolarization of the muscle membrane. During this process, sodium channels open to allow sodium influx, while **potassium ions leak out** of the muscle cells into the extracellular fluid. In a healthy individual, this typically raises serum potassium by **0.5 mEq/L**. However, in patients with burns, massive trauma, or denervation injuries, this rise can be life-threatening. **2. Analysis of Incorrect Options:** * **A. Bradycardia:** Succinylcholine can stimulate muscarinic receptors in the sinus node, leading to bradycardia. This is especially common in children or after a second dose in adults. * **C. Increased Intracranial Tension (ICT):** Depolarization and associated muscle fasciculations can lead to a transient increase in cerebral blood flow and ICT. * **D. Increased Intraocular Pressure (IOP):** Succinylcholine causes a transient rise in IOP (approx. 5-10 mmHg) due to the contraction of extraocular muscles and choroidal vascular dilation. It should be used with caution in penetrating eye injuries. **NEET-PG High-Yield Pearls:** * **Drug of Choice:** Succinylcholine remains the drug of choice for **Rapid Sequence Induction (RSI)** due to its rapid onset (30-60s) and short duration (5-10 mins). * **Metabolism:** It is metabolized by **Pseudocholinesterase** (Plasma cholinesterase). * **Malignant Hyperthermia:** Succinylcholine is a potent trigger for Malignant Hyperthermia. * **Fasciculations:** These are visible muscle twitches caused by initial depolarization, which can lead to postoperative myalgia.

Question 292: Which of the following is a designer drug?

A. Propofol
B. Ketamine (Correct Answer)
C. Alcohol
D. Disulfiram

Explanation: **Explanation:** The term **"Designer Drug"** refers to synthetic analogs of controlled substances that are chemically modified to mimic the pharmacological effects of the original drug while initially circumventing legal restrictions. In the context of anesthesiology and forensic medicine, **Ketamine** is classified as a designer drug (specifically a dissociative anesthetic) because it is a synthetic derivative of **Phencyclidine (PCP)**. * **Ketamine (Correct):** It was synthesized as a safer alternative to PCP. It acts primarily as an NMDA receptor antagonist, producing "dissociative anesthesia" characterized by analgesia, amnesia, and a trance-like state. Due to its hallucinogenic properties, it is frequently used recreationally (often called "Special K"). * **Propofol (Incorrect):** This is a substituted isopropylphenol used for induction and maintenance of anesthesia. While it is a synthetic sedative-hypnotic, it is not a structural analog of a controlled substance designed to bypass laws. * **Alcohol (Incorrect):** Ethanol is a naturally occurring fermentation product and a legal substance (in most jurisdictions), not a synthetic "designer" modification of another drug. * **Disulfiram (Incorrect):** This is an aldehyde dehydrogenase inhibitor used as an aversive therapy for alcohol dependence. It is a therapeutic agent, not a recreational designer drug. **High-Yield Clinical Pearls for NEET-PG:** * **Ketamine** is the only intravenous anesthetic that possesses **analgesic** properties and causes **sympathetic stimulation** (increases HR, BP, and CO). * It is the drug of choice for induction in **bronchial asthma** (due to bronchodilation) and **hypovolemic shock**. * **Emergence delirium** is a common side effect, which can be mitigated by pre-treatment with benzodiazepines (e.g., Midazolam). * It is contraindicated in patients with increased intracranial pressure (ICP) or intraocular pressure.

Question 293: What is the dose of thiopentone used for induction?

A. 1 mg/kg
B. 2 mg/kg
C. 5 mg/kg (Correct Answer)
D. 10 mg/kg

Explanation: **Explanation:** Thiopentone sodium is an ultra-short-acting barbiturate that has long been the "gold standard" induction agent in anesthesia. The standard intravenous induction dose for a healthy adult is **3–5 mg/kg** (commonly cited as **5 mg/kg** in exams). **Why Option C is correct:** At a dose of 5 mg/kg, thiopentone rapidly crosses the blood-brain barrier due to its high lipid solubility, causing loss of consciousness within one arm-brain circulation time (approx. 30 seconds). Its action is terminated by **redistribution** from the brain to lean tissues (muscle and fat), rather than metabolism. **Why other options are incorrect:** * **A (1 mg/kg):** This is a sub-therapeutic dose for induction. However, small doses (0.5–1 mg/kg) may be used to treat intractable seizures or to relieve pruritus associated with spinal opioids. * **B (2 mg/kg):** This is the standard induction dose for **Propofol** (1.5–2.5 mg/kg) or **Etomidate** (0.3 mg/kg), but insufficient for reliable induction with Thiopentone. * **D (10 mg/kg):** This dose is excessive and can lead to severe cardiovascular depression, profound hypotension, and prolonged respiratory apnea. **High-Yield Clinical Pearls for NEET-PG:** * **Preparation:** It is stored as a yellow powder (mixed with 6% anhydrous sodium carbonate to prevent precipitation) and reconstituted as a **2.5% solution**. * **Contraindication:** It is strictly contraindicated in **Porphyria** (induces ALA synthetase). * **Complication:** Intra-arterial injection causes severe vasospasm and gangrene. Treatment includes injecting **Papaverine**, Lidocaine, or performing a Stellate ganglion block. * **Context:** It provides excellent **cerebral protection** by decreasing the cerebral metabolic rate of oxygen (CMRO2) and intracranial pressure (ICP).

Question 294: Ketamine is contraindicated in which of the following conditions?

A. Ischemic heart disease (Correct Answer)
B. Bronchial asthma
C. Shock
D. Tetralogy of Fallot

Explanation: **Explanation:** **Ketamine** is a unique intravenous anesthetic agent that acts as a **direct myocardial depressant** but an **indirect sympathomimetic**. It inhibits the reuptake of catecholamines, leading to increased heart rate, cardiac output, and arterial blood pressure. 1. **Why Ischemic Heart Disease (IHD) is the correct answer:** The sympathomimetic effects of Ketamine significantly increase **myocardial oxygen demand**. In patients with IHD, the coronary arteries cannot meet this increased demand, potentially precipitating myocardial ischemia, infarction, or heart failure. Therefore, it is strictly contraindicated in IHD and severe hypertension. 2. **Why the other options are incorrect:** * **Bronchial Asthma:** Ketamine is the **induction agent of choice** for asthmatics because it causes bronchodilation (via catecholamine release) and preserves airway reflexes. * **Shock:** Ketamine is the **induction agent of choice in hypovolemic/hemorrhagic shock** because its pressor effects help maintain blood pressure (provided catecholamine stores are not exhausted). * **Tetralogy of Fallot (TOF):** Ketamine is preferred in cyanotic heart diseases like TOF because it increases Systemic Vascular Resistance (SVR), which reduces the right-to-left shunt and improves oxygenation. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** NMDA receptor antagonist. * **Dissociative Anesthesia:** Characterized by a "trance-like" state, eyes remaining open with a slow nystagmic gaze. * **Hallucinations:** "Emergence delirium" is a common side effect, which can be minimized by co-administering Benzodiazepines (e.g., Midazolam). * **Intracranial Pressure (ICP):** Traditionally contraindicated in head injuries as it increases ICP and Intraocular pressure (IOP). * **Secretions:** It causes significant salivation (Sialagogue effect); premedication with Glycopyrrolate is often required.

Question 295: Which anesthetic agent is known for providing a smooth induction?

A. Diethyl ether
B. Isoflurane
C. Nitrous oxide
D. Halothane (Correct Answer)

Explanation: **Explanation:** The "smoothness" of an inhalational induction is primarily determined by the **non-irritant nature** of the gas on the airway and its **pleasant odor**. **Why Halothane is Correct:** Halothane is the classic agent of choice for smooth inhalational induction, particularly in pediatric anesthesia. It is **non-pungent**, sweet-smelling, and does not irritate the respiratory mucosa. This prevents complications like coughing, breath-holding, or laryngospasm during the induction phase. While Sevoflurane has largely replaced it in modern practice due to a faster onset (lower blood-gas solubility), Halothane remains the historically correct answer for its lack of pungency. **Analysis of Incorrect Options:** * **Diethyl ether:** Highly pungent and irritating to the airways. It causes significant secretions and a prolonged, stormy induction (Stage II of anesthesia). * **Isoflurane:** Known for its **pungency**. It is a potent airway irritant that can trigger coughing and laryngospasm, making it unsuitable for mask induction. * **Nitrous oxide:** While non-irritating, it is an incomplete anesthetic (MAC > 100%). It is used as an adjuvant to speed up induction (Second Gas Effect) but cannot provide smooth induction as a standalone agent. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard for Induction:** In modern practice, **Sevoflurane** is the preferred agent for smooth induction due to low pungency and rapid onset. * **Halothane Hepatitis:** A rare but serious post-operative complication caused by the metabolite trifluoroacetylated liver proteins. * **Arrhythmogenic Potential:** Halothane sensitizes the myocardium to catecholamines, increasing the risk of arrhythmias. * **Pungent Agents (Avoid for induction):** Desflurane and Isoflurane.

Question 296: Which of the following statements is/are false?

A. Enflurane interacts with sodalime.
B. Sevoflurane causes seizures.
C. Rapid recovery from propofol.
D. All of the above. (Correct Answer)

Explanation: This question tests your knowledge of the clinical properties and side-effect profiles of common anesthetic agents. The correct answer is **D (All of the above)** because each individual statement provided is clinically inaccurate. ### **Detailed Analysis** * **Option A (Enflurane interacts with sodalime):** This is **False**. **Sevoflurane** is the agent notorious for interacting with soda lime (strong bases) to produce **Compound A**, which is nephrotoxic in rats. Enflurane is stable in soda lime. However, Enflurane is known for being metabolized to inorganic fluoride, which can be nephrotoxic. * **Option B (Sevoflurane causes seizures):** This is **False**. While Sevoflurane can show epileptiform patterns on an EEG (especially during mask induction in children), it does not typically cause clinical seizures. In fact, **Enflurane** is the volatile anesthetic most classically associated with inducing seizure-like activity (tonic-clonic movements) and spike-and-wave patterns on EEG, especially under conditions of hypocapnia. * **Option C (Rapid recovery from propofol):** This is **False** in the context of comparison. While Propofol has a rapid onset and a short initial distribution half-life, its "recovery" (emergence) is actually **slower** than that of the ultra-short-acting agent **Remifentanil** or the newer volatile agents like **Desflurane** (which has the lowest blood-gas solubility). Furthermore, in the context of this specific MCQ format, it is often contrasted with agents that have even faster offset kinetics. ### **High-Yield NEET-PG Pearls** * **Compound A:** Associated with Sevoflurane + Soda Lime (worsened by low-flow anesthesia). * **Carbon Monoxide (CO) Production:** Occurs when Desflurane or Isoflurane passes through **dry/desiccated** soda lime. * **Drug of Choice for Day Care Surgery:** Propofol (due to clear-headed recovery and anti-emetic properties). * **Epilepsy-safe agents:** Isoflurane and Thiopentone (Thiopentone is a potent anticonvulsant). * **Avoid Enflurane in:** Patients with a history of epilepsy or renal failure.

Question 297: Minimum alveolar concentration (MAC) is a measure of:

A. Potency of an anesthetic agent (Correct Answer)
B. Speed of induction and recovery
C. Lipid solubility of an agent
D. Toxicity of an agent

Explanation: **Explanation** **1. Why Option A is Correct:** Minimum Alveolar Concentration (MAC) is defined as the concentration of an inhaled anesthetic at 1 atmosphere (at steady state) that prevents skeletal muscle movement in response to a noxious stimulus (like a surgical skin incision) in 50% of patients. In pharmacology, **potency** is inversely proportional to the dose required to achieve a specific effect. Therefore, an anesthetic with a **low MAC is highly potent** (e.g., Halothane), while one with a **high MAC has low potency** (e.g., Nitrous Oxide). **2. Why Other Options are Incorrect:** * **Option B (Speed of induction/recovery):** This is determined by the **Blood-Gas Partition Coefficient**. Agents with low solubility in blood (e.g., Desflurane) result in faster induction and recovery. * **Option C (Lipid solubility):** While the **Meyer-Overton Hypothesis** states that potency correlates with lipid solubility (Oil-Gas Partition Coefficient), MAC itself is the *measure* of potency, not the solubility. * **Option D (Toxicity):** Toxicity is related to the metabolic byproducts of the agent (e.g., Compound A from Sevoflurane or fluoride ions) and is not measured by MAC. **3. High-Yield Clinical Pearls for NEET-PG:** * **MAC Values:** Halothane (0.75%), Isoflurane (1.15%), Sevoflurane (2%), Desflurane (6%), Nitrous Oxide (104%). * **MAC-Awake:** The concentration at which 50% of patients respond to verbal commands (usually ~0.3–0.4 MAC). * **MAC-BAR:** The concentration required to block autonomic responses to incision (~1.5 MAC). * **Factors increasing MAC (Higher dose needed):** Hyperthermia, hypernatremia, chronic alcohol abuse, and young age (highest at 6 months). * **Factors decreasing MAC (Lower dose needed):** Hypothermia, hyponatremia, pregnancy, acute alcohol intoxication, old age, and opioids/sedatives.

Question 298: Which of the following is true in relation to Ethylene glycol poisoning?

A. It may present with an acute ascending motor and sensory neuropathy. (Correct Answer)
B. A normal anion gap acidosis is usually seen.
C. Alcohol dehydrogenase metabolizes Ethylene glycol into metabolites including oxalate and glycolic acid.
D. Hemodialysis is not effective.

Explanation: **Explanation:** **1. Why Option A is Correct:** Ethylene glycol poisoning typically presents in three stages: neurological, cardiopulmonary, and renal. While the early phase mimics ethanol intoxication, a delayed neurological manifestation (occurring 5–20 days post-ingestion) can involve **cranial nerve palsies** (especially facial nerve) and an **acute ascending motor and sensory neuropathy** similar to Guillain-Barré Syndrome. This is thought to be due to the deposition of calcium oxalate crystals in the vasa nervorum or direct toxic effects of metabolites. **2. Why Incorrect Options are Wrong:** * **Option B:** Ethylene glycol poisoning is a classic cause of a **High Anion Gap Metabolic Acidosis (HAGMA)**. The accumulation of glycolic acid and lactic acid leads to a significant drop in bicarbonate and an increased anion gap. * **Option C:** This statement is partially true but technically incomplete/distorted in the context of the "best" answer. While Alcohol Dehydrogenase (ADH) is the rate-limiting enzyme, it converts ethylene glycol into **glycoaldehyde**, which is then further metabolized by other enzymes into glycolic acid, glyoxylic acid, and finally **oxalate**. * **Option D:** Hemodialysis is **highly effective** and often the definitive treatment. It removes both the parent compound (ethylene glycol) and its toxic metabolites (glycolic acid) while correcting the metabolic acidosis. **3. High-Yield Clinical Pearls for NEET-PG:** * **Antidote:** Fomepizole (inhibits ADH) is the first-line treatment. Ethanol is an alternative. * **Diagnostic Clue:** Presence of **envelope-shaped calcium oxalate crystals** in the urine (crystalluria). * **Osmolar Gap:** Ethylene glycol causes a high osmolar gap early in the ingestion before it is fully metabolized. * **Mnemonic for HAGMA:** MUDPILES (M-Methanol, U-Uremia, D-DKA, P-Paraldehyde, **I-Isoniazid/Iron**, L-Lactic acidosis, **E-Ethylene glycol**, S-Salicylates).

Question 299: Nitrous oxide is contraindicated in patients with pneumothorax, pneumopericardium, or intestinal obstruction because it:

A. Depresses an already compromised myocardium
B. Permits the use of limited FIO2 only
C. Is less soluble than nitrogen
D. Causes the expansion of air-filled body cavities (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Causes the expansion of air-filled body cavities.** This phenomenon is based on the **Blood-Gas Partition Coefficient**. Nitrous oxide ($N_2O$) is 34 times more soluble in blood than Nitrogen ($N_2$). When $N_2O$ is administered, it diffuses from the blood into air-filled spaces much faster than $N_2$ can diffuse out of those spaces into the blood. This leads to a rapid increase in the volume (if the cavity is compliant, like the bowel) or pressure (if the cavity is non-compliant, like the middle ear or skull) of the air-filled space. In conditions like **pneumothorax**, $N_2O$ can double the size of the pocket in 10 minutes, potentially leading to a tension pneumothorax. In **intestinal obstruction**, it worsens distension, making surgical closure difficult and increasing the risk of ischemia. **Analysis of Incorrect Options:** * **A:** While $N_2O$ has a mild direct myocardial depressant effect, it is usually offset by sympathetic stimulation. This is not the primary reason for its contraindication in these specific surgical conditions. * **B:** While using $N_2O$ limits the maximum $FiO_2$ (as it occupies a percentage of the gas mixture), this is a general limitation of the gas, not the specific reason it is contraindicated in closed-space pathologies. * **C:** This is factually incorrect. $N_2O$ is significantly **more** soluble than Nitrogen, which is the physiological basis for the expansion of cavities. **High-Yield Clinical Pearls for NEET-PG:** * **Contraindications for $N_2O$:** Pneumothorax, air embolism, intestinal obstruction, intraocular gas bubbles (sulfur hexafluoride), tympanoplasty, and recent neurosurgery (pneumocephalus). * **Diffusion Hypoxia (Fink Effect):** Occurs at the end of anesthesia when $N_2O$ rushes out of the blood into the alveoli, diluting oxygen. Prevented by giving 100% $O_2$ for 5–10 minutes post-discontinuation. * **Second Gas Effect:** $N_2O$ speeds up the uptake of a companion volatile anesthetic. * **Vitamin B12:** $N_2O$ irreversibly oxidizes the cobalt atom in Vitamin B12, inhibiting methionine synthase. Prolonged exposure can lead to megaloblastic anemia or myeloneuropathy.

Question 300: Which of the following inhalational agents is the most soluble in blood?

A. Halothane (Correct Answer)
B. Isoflurane
C. Enflurane
D. Desflurane

Explanation: The speed of induction and recovery from inhalational anesthesia is primarily determined by the **Blood-Gas Partition Coefficient**. This value represents the solubility of the anesthetic agent in the blood relative to the alveolar gas. ### 1. Why Halothane is Correct **Halothane** has a Blood-Gas Partition Coefficient of approximately **2.3 to 2.54**. Among the options provided, this is the highest value. High blood solubility means the agent dissolves extensively in the blood, acting as a large reservoir. This results in a slower rise in the partial pressure of the anesthetic in the alveoli and brain, leading to a **slower induction and recovery** compared to less soluble agents. ### 2. Analysis of Incorrect Options * **Enflurane (BGP ~1.8-1.9):** It is less soluble than Halothane but more soluble than Isoflurane. * **Isoflurane (BGP ~1.4):** It has intermediate solubility. While it is a commonly used maintenance agent, it is significantly less soluble than Halothane. * **Desflurane (BGP ~0.42):** This is the **least soluble** agent among the options. Low solubility allows for the fastest induction and the most rapid emergence from anesthesia. ### 3. NEET-PG High-Yield Pearls * **Solubility vs. Speed:** Solubility is **inversely proportional** to the speed of induction. (High Solubility = Slow Induction; Low Solubility = Fast Induction). * **Potency:** Potency is determined by the **MAC (Minimum Alveolar Concentration)**. Halothane has the lowest MAC (~0.75%), making it the most potent agent listed. * **Order of Solubility (Highest to Lowest):** Ether (12) > Halothane (2.4) > Enflurane (1.9) > Isoflurane (1.4) > Sevoflurane (0.65) > Nitrous Oxide (0.47) > Desflurane (0.42). * **Clinical Note:** Halothane is rarely used in modern practice due to the risk of "Halothane Hepatitis" and its tendency to sensitize the myocardium to catecholamines (arrhythmogenic).

Practice by Chapter

History of Anesthesia

Practice Questions

Preoperative Evaluation

Practice Questions

Pharmacology of Inhalational Anesthetics

Practice Questions

Pharmacology of Intravenous Anesthetics

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Neuromuscular Blocking Agents

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Airway Management

Practice Questions

Endotracheal Intubation

Practice Questions

Difficult Airway Algorithms

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Intraoperative Monitoring

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Depth of Anesthesia Monitoring

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Emergence from Anesthesia

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Postoperative Care

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