General Anesthesia Practice Questions

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

Propofol. **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).

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

Quinidine. **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.

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

Rapacuronium. **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.

Q: Which anesthetic agent is contraindicated in acute hepatitis?

Halothane. **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).

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

It is an intermediate-acting barbiturate.. **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.

Q: Suxamethonium is which of the following?

A depolarizing muscle relaxant. **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).

Q: What is the primary use of dexmedetomidine?

As a sedative agent for intubated patients.. **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).

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

Lorazepam. **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.

Question 1

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

Accepted Answer

Propofol

Answer

Midazolam

Answer

Ketamine

Answer

Thiopentone sodium

Question 2

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

Accepted Answer

Quinidine

Answer

Hyperkalemia

Answer

Hypomagnesemia

Answer

Chronic phenytoin therapy

Question 3

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

Accepted Answer

Rapacuronium

Answer

Succinylcholine

Answer

Atracurium

Answer

Pancuronium

Question 4

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

Accepted Answer

Diaphragmatic relaxation

Answer

Abdominal wall relaxation

Answer

Diplopia

Answer

Ptosis

Question 5

Which anesthetic agent is contraindicated in acute hepatitis?

Accepted Answer

Halothane

Answer

Sevoflurane

Answer

Ketamine

Answer

Isoflurane

Question 6

Which of the following is NOT true about thiopental sodium?

Accepted Answer

It is an intermediate-acting barbiturate.

Answer

It is cerebroprotective.

Answer

It is an agent of choice for narcoanalysis.

Answer

It is contraindicated in acute intermittent porphyria.

Question 7

Suxamethonium is which of the following?

Accepted Answer

A depolarizing muscle relaxant

Answer

A non-depolarizing muscle relaxant

Answer

A direct-acting muscle relaxant

Answer

All of the above

Question 8

Thiopentone is contraindicated in all except?

Accepted Answer

Porphyria cutanea tarda

Answer

Status asthmaticus

Answer

Shock

Answer

Acute intermittent porphyria

Question 9

What is the primary use of dexmedetomidine?

Accepted Answer

As a sedative agent for intubated patients.

Answer

To prolong the action of local anesthetics in hypertensive patients.

Answer

To increase the bioavailability of regional anesthetic drugs.

Answer

To reduce the bispectral index of general anesthetic drugs with low potency.

Question 10

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

Accepted Answer

Lorazepam

Answer

Bupivacaine

Answer

Neostigmine

Answer

Dexmedetomidine

General Anesthesia — MCQs

General Anesthesia — MCQs

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