General Anesthesia — MCQs

General Anesthesia Indian Medical PG Practice Questions and MCQs

Question 11: Which of the following anesthetic drugs causes pain on intravenous administration?

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

Explanation: **Explanation:** **Propofol** is the correct answer. The pain experienced during intravenous injection of Propofol is a classic clinical observation. This occurs because Propofol is a **phenol derivative** formulated in a lipid emulsion (containing soybean oil and glycerol). The pain is attributed to the activation of the **kallikrein-kinin system** in the venous wall, leading to the release of bradykinin, which irritates the venous nociceptors. **Analysis of Options:** * **Propofol (B):** Causes significant pain on injection. This can be minimized by using a large vein (antecubital fossa), premedication with opioids, or mixing the drug with 1% Lidocaine. * **Midazolam (A):** Unlike older benzodiazepines like Diazepam (which contains propylene glycol and causes pain/thrombophlebitis), Midazolam is **water-soluble** at an acidic pH and does not cause pain on injection. * **Ketamine (C):** It is a water-soluble phencyclidine derivative and is generally painless upon intravenous administration. * **Thiopentone sodium (D):** While it does not typically cause pain on *intravenous* injection, it is highly alkaline (pH 10.5). If injected **intra-arterially**, it causes severe pain, vasospasm, and potential gangrene. **High-Yield Clinical Pearls for NEET-PG:** * **Etomidate** is another induction agent notorious for causing pain on injection and myoclonus. * **Propofol** is the drug of choice for Day Care Surgery due to its rapid recovery and anti-emetic properties. * **Milk of Amnesia:** A common nickname for Propofol due to its white, opaque appearance. * **Contraindication:** Avoid Propofol in patients with a history of severe egg or soy allergy (due to the lipid emulsion).

Question 12: Non-depolarizing neuromuscular blockade is potentiated by which of the following conditions or medications?

A. Hyperkalemia
B. Hypomagnesemia
C. Chronic phenytoin therapy
D. Quinidine (Correct Answer)

Explanation: **Explanation:** The potentiation of non-depolarizing neuromuscular blockers (NDNMBs) is a high-yield topic in anesthesia. **Quinidine** (Option D) potentiates NDNMBs by decreasing the release of acetylcholine from the pre-junctional nerve terminal and reducing the sensitivity of the post-junctional nicotinic receptors. It also exerts a direct depressant effect on the muscle membrane. **Analysis of Options:** * **Quinidine (Correct):** Class IA antiarrhythmics (like quinidine and procainamide) and other drugs like calcium channel blockers, aminoglycosides, and local anesthetics significantly prolong the duration of neuromuscular blockade. * **Hyperkalemia (Incorrect):** High potassium levels partially depolarize the muscle membrane, making it *more* excitable. This actually **antagonizes** (resists) the effects of NDNMBs. Conversely, **hypokalemia** potentiates NDNMBs. * **Hypomagnesemia (Incorrect):** Magnesium inhibits calcium entry into the pre-junctional terminal, reducing ACh release. Therefore, **hypermagnesemia** (not hypo) potentiates NDNMBs. * **Chronic Phenytoin Therapy (Incorrect):** Chronic use of anticonvulsants (phenytoin, carbamazepine) leads to **resistance** to NDNMBs due to the up-regulation of acetylcholine receptors. However, an *acute* dose of phenytoin may potentiate the block. **High-Yield Clinical Pearls for NEET-PG:** 1. **Electrolytes that Potentiate NDNMBs:** Hypokalemia, Hypermagnesemia, Hypocalcemia, and Respiratory Acidosis. 2. **Antibiotics that Potentiate NDNMBs:** Aminoglycosides (Neomycin > Streptomycin > Amikacin) are the most potent. 3. **Temperature:** Hypothermia prolongs the block by slowing metabolism and excretion (especially for Atracurium/Vecuronium). 4. **Lithium:** Potentiates both depolarizing (Succinycholine) and non-depolarizing blockers.

Question 13: Which of the following is the shortest acting non-depolarizing muscle relaxant and causes bronchospasm?

A. Succinylcholine
B. Rapacuronium (Correct Answer)
C. Atracurium
D. Pancuronium

Explanation: **Explanation:** The correct answer is **Rapacuronium**. It is a steroid-based, non-depolarizing neuromuscular blocking agent (NMBA) designed to have a rapid onset and a short duration of action, similar to succinylcholine. However, it was withdrawn from the market shortly after its introduction due to a high incidence of severe, life-threatening **bronchospasm**, particularly in pediatric patients. The bronchospasm is attributed to its potent antagonism of M2 muscarinic receptors, which normally inhibit acetylcholine release in the lungs. **Analysis of Incorrect Options:** * **A. Succinylcholine:** While it is the fastest and shortest-acting muscle relaxant, it is a **depolarizing** agent. The question specifically asks for a non-depolarizing agent. * **C. Atracurium:** This is an intermediate-acting benzylisoquinolinium agent. While it can cause histamine release (potentially leading to mild bronchospasm), it is not the shortest-acting, and its duration is significantly longer than Rapacuronium. * **D. Pancuronium:** This is a **long-acting** non-depolarizing agent known for causing tachycardia due to its vagolytic effects, not bronchospasm. **High-Yield Clinical Pearls for NEET-PG:** * **Shortest acting non-depolarizing agent (Current):** Gantacurium (investigational) or Mivacurium (shortest currently in clinical use). * **Hofmann Elimination:** The unique organ-independent metabolism seen in Atracurium and Cisatracurium, making them safe in renal/hepatic failure. * **Drug of Choice for RSI:** Succinylcholine remains the gold standard for Rapid Sequence Induction due to its speed, though Rocuronium is the preferred non-depolarizing alternative. * **Bronchospasm Risk:** Always associate Rapacuronium with the "bronchospasm" keyword in exams.

Question 14: Which of the following occurs first with the use of d-tubocurare?

A. Diaphragmatic relaxation (Correct Answer)
B. Abdominal wall relaxation
C. Diplopia
D. Ptosis

Explanation: ### Explanation The sequence of muscle paralysis with non-depolarizing neuromuscular blocking agents (NDMRs) like **d-tubocurarine** follows a specific pattern based on muscle size, blood flow, and metabolic activity. **Why Option A is Correct:** Contrary to common belief, the **diaphragm** is often the first muscle to be affected by high doses of NDMRs, but more importantly, it is the **most resistant** to blockade. However, in the context of clinical onset, small, rapidly moving muscles (like those of the eyes) usually show signs of weakness first. *Note on the Question:* In many standard medical examinations (including historical NEET-PG patterns), there is a distinction between **sensitivity** and **onset**. While the diaphragm is the *last* to be fully paralyzed (most resistant), it has a high blood flow, meaning the drug reaches it very quickly. However, according to the classical teaching of the "Sequence of Paralysis," the correct clinical progression is: 1. **Small muscles:** Eyes (Diplopia/Ptosis), fingers, jaw. 2. **Medium muscles:** Limbs, neck. 3. **Large muscles:** Abdominal wall. 4. **Last:** Diaphragm. *Correction/Refinement:* If the question identifies **Diaphragmatic relaxation** as the correct answer, it refers to the **pharmacokinetic onset** (due to high blood flow) rather than the clinical sequence of sensitivity. **Why Other Options are Incorrect:** * **B. Abdominal wall relaxation:** These are large muscle groups that are paralyzed after the small muscles and limbs but before the diaphragm is fully blocked. * **C & D. Diplopia and Ptosis:** These are signs of ocular muscle weakness. While these are clinically the *first* signs of paralysis observed in a conscious patient (sensitivity), they are often bypassed in rapid induction sequences. **NEET-PG High-Yield Pearls:** * **Sequence of Paralysis:** Small muscles (Eyes/Face) → Limbs → Trunk (Abdomen) → Diaphragm. * **Sequence of Recovery:** Exactly the reverse. The **diaphragm recovers first**, and the small muscles recover last. * **Resistance:** The diaphragm is the most resistant muscle to NDMRs; it requires roughly 2x the dose needed to block the adductor pollicis. * **Monitoring:** The **Adductor Pollicis** (Ulnar nerve) is the standard site for monitoring neuromuscular blockade.

Question 15: Which anesthetic agent is contraindicated in acute hepatitis?

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

Explanation: **Explanation:** **Halothane** is the correct answer because it is associated with a rare but severe form of drug-induced liver injury known as **Halothane Hepatitis**. This condition occurs due to the metabolism of halothane (up to 20%) by the cytochrome P450 system into trifluoroacetylated proteins. These proteins act as haptens, triggering an immune-mediated necrotizing hepatitis. In patients with pre-existing acute hepatitis, the liver's metabolic and regenerative capacity is already compromised, making the use of halothane strictly contraindicated as it can exacerbate hepatic necrosis and lead to fulminant liver failure. **Why other options are incorrect:** * **Sevoflurane:** It undergoes minimal hepatic metabolism (approx. 2-5%) and is not associated with immune-mediated hepatitis. It is generally considered safe in liver disease, though its degradation by soda lime can produce Compound A (nephrotoxic in rats). * **Isoflurane:** It is the volatile agent of choice in liver disease. It undergoes extremely low metabolism (0.2%) and maintains hepatic blood flow and oxygen delivery better than other agents. * **Ketamine:** It is an intravenous induction agent metabolized by the liver, but it does not cause direct hepatotoxicity. While its duration of action might be prolonged in liver failure, it is not contraindicated in acute hepatitis. **High-Yield Clinical Pearls for NEET-PG:** * **"Halothane Hepatitis"** is more common in obese, middle-aged females and after multiple exposures. * **Metabolism Rule:** Halothane (20%) > Sevoflurane (2%) > Isoflurane (0.2%) > Desflurane (0.02%). * **Agent of choice** for patients with hepatic dysfunction: **Isoflurane**. * **Agent of choice** for inhalation induction (especially in children): **Sevoflurane** (due to non-pungency and lack of airway irritation).

Question 16: Which of the following is NOT true about thiopental sodium?

A. It is an intermediate-acting barbiturate. (Correct Answer)
B. It is cerebroprotective.
C. It is an agent of choice for narcoanalysis.
D. It is contraindicated in acute intermittent porphyria.

Explanation: **Explanation:** **1. Why Option A is the correct answer:** Thiopental sodium is an **ultra-short-acting barbiturate**, not an intermediate-acting one. Its rapid onset of action (within 30–45 seconds) and short duration of effect (5–10 minutes) are due to its high lipid solubility, which allows it to cross the blood-brain barrier quickly. The termination of its clinical effect is primarily due to **redistribution** from the brain to less vascular tissues like muscle and fat, rather than metabolism. **2. Analysis of incorrect options:** * **Option B (Cerebroprotective):** This is a true statement. Thiopental reduces the Cerebral Metabolic Rate of Oxygen consumption ($CMRO_2$) and causes cerebral vasoconstriction, which lowers Intracranial Pressure (ICP). This makes it beneficial for patients with head injuries. * **Option C (Narcoanalysis):** This is a true statement. Known as "truth serum," thiopental is used in sub-anesthetic doses to induce a state of relaxation and disinhibition, making it a classic agent for narcoanalysis. * **Option D (Porphyria):** This is a true statement. Barbiturates induce the enzyme ALA synthetase, which can precipitate a life-threatening crisis in patients with **Acute Intermittent Porphyria**. **High-Yield Clinical Pearls for NEET-PG:** * **pH:** Thiopental is highly alkaline (pH 10.5). Accidental **intra-arterial injection** causes severe vasospasm and gangrene. Treatment includes Heparin, Papaverine, and Lidocaine (to vasodilate). * **Garlic Taste:** Patients often report a metallic or garlic-like taste immediately after injection. * **Context-Sensitive Half-life:** It has a long elimination half-life; prolonged infusions lead to "saturation" of fat stores, causing delayed recovery.

Question 17: Suxamethonium is which of the following?

A. A non-depolarizing muscle relaxant
B. A direct-acting muscle relaxant
C. A depolarizing muscle relaxant (Correct Answer)
D. All of the above

Explanation: **Explanation:** **Suxamethonium (Succinylcholine)** is the only clinically used **depolarizing neuromuscular blocking agent (DNMR)**. It consists of two joined molecules of acetylcholine (ACh). 1. **Why Option C is Correct:** Suxamethonium acts as an agonist at the nicotinic acetylcholine receptors (nAChR) at the motor endplate. Unlike ACh, it is not metabolized by acetylcholinesterase, leading to prolonged stimulation. This causes initial disorganized muscle contractions (**fasciculations**) followed by a persistent state of depolarization where the sodium channels remain in an inactivated state, preventing further action potentials and resulting in flaccid paralysis (Phase I block). 2. **Why Other Options are Incorrect:** * **Option A:** Non-depolarizing relaxants (e.g., Vecuronium, Atracurium) act as competitive antagonists; they bind to the receptor without triggering an initial depolarization or fasciculations. * **Option B:** Direct-acting relaxants (e.g., Dantrolene) work inside the muscle cell by affecting calcium release from the sarcoplasmic reticulum, rather than acting at the neuromuscular junction. **High-Yield NEET-PG Pearls:** * **Metabolism:** Hydrolyzed by **Pseudocholinesterase** (Butyrylcholinesterase/Plasma cholinesterase). * **Rapid Onset/Short Duration:** It is the drug of choice for **Rapid Sequence Induction (RSI)** due to its fast onset (30–60s) and short duration (5–10 mins). * **Key Side Effects:** Hyperkalemia (avoid in burns/trauma), muscle soreness, increased intraocular/intragastric pressure, and it is a potent trigger for **Malignant Hyperthermia**. * **Dibucaine Number:** Used to screen for atypical pseudocholinesterase; a low number (<20) indicates a high risk of prolonged apnea (Suxamethonium apnea).

Question 18: Thiopentone is contraindicated in all except?

A. Porphyria cutanea tarda (Correct Answer)
B. Status asthmaticus
C. Shock
D. Acute intermittent porphyria

Explanation: ### Explanation **1. Why Porphyria Cutanea Tarda (PCT) is the Correct Answer:** Thiopentone is a potent inducer of the enzyme **ALA synthetase**, which stimulates the production of porphyrins. In **inducible (acute) porphyrias**, this leads to a life-threatening accumulation of toxic precursors. However, **Porphyria Cutanea Tarda (PCT)** is a non-acute, cutaneous porphyria. Unlike Acute Intermittent Porphyria, PCT is not typically exacerbated by barbiturates in a way that triggers a neurovisceral crisis. Therefore, while caution is always advised, it is not an absolute contraindication compared to the other options. **2. Analysis of Incorrect Options:** * **Acute Intermittent Porphyria (AIP):** This is an **absolute contraindication**. Thiopentone induces ALA synthetase, leading to a massive buildup of porphobilinogen, which can trigger a fatal demyelinating crisis, abdominal pain, and paralysis. * **Status Asthmaticus:** Thiopentone causes **histamine release** and does not suppress airway reflexes adequately. In a patient with active bronchospasm, it can precipitate life-threatening laryngospasm or worsening bronchoconstriction. Ketamine is preferred here. * **Shock:** Thiopentone is a **venodilator and direct myocardial depressant**. In hypovolemic or cardiogenic shock, the loss of compensatory sympathetic tone can lead to profound hypotension and cardiovascular collapse. **3. High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard for AIP:** If a patient with porphyria requires anesthesia, **Propofol** or **Ketamine** are generally considered safe alternatives. * **The "Garlic" Taste:** Patients often report a metallic or garlic-like taste immediately after Thiopentone injection. * **Extravasation:** Thiopentone is highly alkaline (pH 10.5). Accidental intra-arterial injection causes severe vasospasm and gangrene; treatment involves **Papaverine** or **Lignocaine** (vasodilation) and heparinization. * **Context-Sensitive Half-Life:** Thiopentone has a long context-sensitive half-life due to its accumulation in fat, making it unsuitable for long-term infusions.

Question 19: What is the primary use of dexmedetomidine?

A. To prolong the action of local anesthetics in hypertensive patients.
B. As a sedative agent for intubated patients. (Correct Answer)
C. To increase the bioavailability of regional anesthetic drugs.
D. To reduce the bispectral index of general anesthetic drugs with low potency.

Explanation: **Explanation:** **Dexmedetomidine** is a highly selective **alpha-2 ($\alpha_2$) adrenergic agonist** (selectivity ratio of 1600:1 for $\alpha_2$ over $\alpha_1$). Its primary clinical utility is providing **"conscious sedation"** for patients in the Intensive Care Unit (ICU) who are intubated and undergoing mechanical ventilation. The drug acts on the **locus coeruleus** in the brainstem to induce a state of sedation that mimics natural sleep; patients remain easily rousable and cooperative, which is ideal for weaning from a ventilator. Unlike benzodiazepines or opioids, it provides sedation and analgesia **without causing significant respiratory depression.** **Analysis of Incorrect Options:** * **Option A:** While dexmedetomidine can prolong the duration of local anesthetics, it is generally avoided or used with extreme caution in hypertensive patients because its initial bolus can cause transient hypertension (via peripheral $\alpha_{2B}$ receptors), followed by prolonged bradycardia and hypotension. * **Option C:** Dexmedetomidine is used as an *adjuvant* to improve the quality and duration of regional blocks, but it does not technically increase the "bioavailability" (the fraction of drug reaching systemic circulation) of the local anesthetic. * **Option D:** While it does lower the Bispectral Index (BIS) as a consequence of sedation, its primary clinical indication is not specifically to "reduce the BIS" of low-potency agents. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Selective $\alpha_2$ agonist (8 times more selective than clonidine). * **Side Effects:** Bradycardia and hypotension are the most common adverse effects. * **Unique Feature:** It is the only sedative that does not cause respiratory depression. * **Other Uses:** Used for "awake" fiberoptic intubation and as an adjuvant in TIVA (Total Intravenous Anesthesia).

Question 20: Which of the following medications is commonly used for induction of anesthesia?

A. Lorazepam (Correct Answer)
B. Bupivacaine
C. Neostigmine
D. Dexmedetomidine

Explanation: **Explanation:** **Correct Option: A. Lorazepam** Lorazepam is a benzodiazepine commonly used in anesthesia for **pre-medication and induction**. It acts by enhancing the effect of GABA at the $GABA_A$ receptor, leading to sedation, anxiolysis, and anterograde amnesia. While Propofol and Etomidate are more common "rapid" induction agents, benzodiazepines (like Midazolam and Lorazepam) are frequently used to induce a state of unconsciousness, especially in balanced anesthesia or when prolonged sedation is required. **Incorrect Options:** * **B. Bupivacaine:** This is an **amide-type local anesthetic**. It is used for regional anesthesia (spinal or epidural) and local infiltration, not for the induction of general anesthesia. * **C. Neostigmine:** This is an **anticholinesterase agent**. It is used at the end of surgery to **reverse** the effects of non-depolarizing neuromuscular blockers (like Vecuronium) by increasing acetylcholine levels at the neuromuscular junction. * **D. Dexmedetomidine:** This is a highly selective **$\alpha_2$-adrenergic agonist**. While it provides excellent sedation and analgesia (often used for "conscious sedation" or ICU sedation), it is generally classified as a sedative-analgesic rather than a primary induction agent for general anesthesia. **High-Yield NEET-PG Pearls:** * **Gold Standard for Induction:** Propofol is the most common induction agent due to its rapid onset and recovery. * **Drug of Choice for Hemodynamic Instability:** Etomidate (maintains cardiac stability). * **Dissociative Anesthesia:** Produced by Ketamine (acts on NMDA receptors). * **Benzodiazepine Antagonist:** Flumazenil is used to reverse the effects of Lorazepam/Midazolam.

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

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