General Anesthesia Practice Questions

Q: Which of the following statements is NOT true for propofol?

Contraindicated in porphyria. **Explanation:** Propofol is the most commonly used intravenous induction agent in modern anesthesia. Understanding its pharmacological profile is high-yield for NEET-PG. **Why Option C is the Correct Answer (The "False" Statement):** Propofol is considered **safe** in patients with porphyria. Unlike older barbiturates (like Thiopentone), propofol does not induce the enzyme ALA synthase and is not known to trigger acute porphyric crises. Therefore, it is often the induction agent of choice for these patients. **Analysis of Other Options:** * **A. Painful intravenous administration:** This is a true statement. Propofol is a lipid emulsion that can cause significant pain on injection due to the activation of the kinin system. This is often mitigated by using larger veins or pre-administering lidocaine. * **B. Induction agent:** This is true. Due to its rapid onset (one arm-brain circulation time) and rapid recovery (short context-sensitive half-life), it is the gold standard for induction and TIVA (Total Intravenous Anesthesia). * **D. Antiemetic effect:** This is true. Propofol possesses unique sub-hypnotic antiemetic properties (likely via dopamine D2 receptor antagonism), making it ideal for patients prone to Postoperative Nausea and Vomiting (PONV). **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** For Day-care surgery, Induction, and TIVA. * **Egg/Soy Allergy:** Use with caution as the emulsion contains egg lecithin and soybean oil. * **Propofol Infusion Syndrome (PRIS):** A rare, fatal complication of prolonged high-dose infusion characterized by metabolic acidosis, rhabdomyolysis, and cardiac failure. * **Hemodynamics:** Causes significant peripheral vasodilation and myocardial depression (caution in hypovolemic/shock patients).

Q: Abnormal plasma choline esterase produces apnea due to which of the following?

Suxamethonium. **Explanation:** The correct answer is **Suxamethonium (Succinylcholine)**. **Mechanism and Pathophysiology:** Suxamethonium is a depolarizing neuromuscular blocking agent widely used for rapid sequence induction. It is metabolized by the enzyme **Pseudocholinesterase** (also known as Plasma Cholinesterase or Butyrylcholinesterase). In patients with a genetic variation resulting in **Abnormal Plasma Cholinesterase** (atypical enzyme), the metabolism of Suxamethonium is significantly delayed. This leads to a prolonged neuromuscular block, resulting in extended muscle paralysis and **prolonged apnea**, necessitating continued mechanical ventilation until the drug eventually wears off. **Analysis of Incorrect Options:** * **Halothane & Isoflurane (Options A & D):** These are volatile inhalational anesthetics. Their action is terminated by redistribution and exhalation through the lungs, not by plasma esterases. While Halothane is associated with hepatotoxicity, it does not cause apnea via cholinesterase deficiency. * **Lignocaine (Option B):** This is an amide-type local anesthetic. Amide local anesthetics are metabolized by hepatic microsomal enzymes (Cytochrome P450), whereas ester-type local anesthetics (like Procaine) are metabolized by plasma cholinesterase. **High-Yield Clinical Pearls for NEET-PG:** * **Dibucaine Number:** This is the screening test for atypical cholinesterase. Dibucaine inhibits normal enzyme by 80% and atypical enzyme by only 20%. A **low Dibucaine number** indicates an atypical enzyme. * **Management:** The primary treatment for Suxamethonium apnea is **continued sedation and mechanical ventilation** until muscle power returns. * **Mivacurium:** This is the only non-depolarizing muscle relaxant also metabolized by plasma cholinesterase; its action is also prolonged in these patients.

Q: Which of the following metabolites of Atracurium is responsible for seizures?

Laudanosine. **Explanation:** **Atracurium** is a benzylisoquinolone neuromuscular blocking agent unique for its metabolism via **Hofmann elimination** (a non-enzymatic degradation occurring at physiological pH and temperature) and ester hydrolysis. **Why Laudanosine is the correct answer:** The primary metabolite of Atracurium is **Laudanosine**. Unlike the parent drug, Laudanosine has no neuromuscular blocking activity. However, it is a tertiary amine that readily crosses the blood-brain barrier. At high plasma concentrations, it acts as a **central nervous system stimulant**, which can lower the seizure threshold and potentially induce **seizures**. While this is rarely seen in routine clinical anesthesia, it is a significant concern during prolonged infusions in ICU settings or in patients with hepatic failure (as Laudanosine is metabolized by the liver). **Analysis of Incorrect Options:** * **A. Cis-atracurium:** This is an isomer of atracurium, not a metabolite. It is more potent, produces significantly less laudanosine, and does not cause histamine release. * **B. FK-506 (Tacrolimus):** This is an immunosuppressant used in organ transplants; it has no metabolic relationship with atracurium. * **D. Gallamine:** This is an older long-acting muscle relaxant known for causing tachycardia (due to vagolytic effects), not a metabolite of atracurium. **High-Yield Clinical Pearls for NEET-PG:** * **Hofmann Elimination:** Atracurium and Cis-atracurium are the drugs of choice in **renal and hepatic failure** because their metabolism is independent of organ function. * **Histamine Release:** Atracurium can cause skin flushing, hypotension, and bronchospasm due to histamine release (Cis-atracurium does not). * **Temperature/pH Sensitivity:** Since Hofmann elimination is temperature and pH-dependent, the duration of action of atracurium is prolonged in patients with **hypothermia or acidosis**.

Q: All of the following decrease the mean alveolar concentration (MAC) of inhalational anesthetics except?

Hypothyroidism. **Explanation:** The **Minimum Alveolar Concentration (MAC)** is the concentration of an inhalational anesthetic at 1 atmosphere that prevents skeletal muscle movement in response to a noxious stimulus in 50% of patients. It is a measure of anesthetic potency (Lower MAC = Higher Potency). **Why Hypothyroidism is the Correct Answer:** Contrary to common clinical intuition, **hypothyroidism does not decrease MAC**. While hypothyroid patients may have a decreased cardiac output or slower metabolism, the anesthetic requirement of the brain remains unchanged. Therefore, MAC is independent of thyroid status (both hyper- and hypothyroidism). **Analysis of Incorrect Options (Factors that DO decrease MAC):** * **Hypoxia (Option A):** Severe hypoxia ($PaO_2 95\ mmHg$) exerts a direct narcotic effect on the brain, thereby lowering MAC. * **Hypovolemia (Option D):** Acute hypotension and decreased cerebral perfusion reduce the delivery and requirement of anesthetics, effectively lowering the MAC. **High-Yield Clinical Pearls for NEET-PG:** * **Factors that Decrease MAC:** Old age, pregnancy, acute ethanol ingestion, hyponatremia, hypothermia, and drugs like opioids, benzodiazepines, and $\alpha_2$ agonists (Clonidine/Dexmedetomidine). * **Factors that Increase MAC:** Young age (highest at 6 months), hypernatremia, hyperthermia, chronic ethanol abuse, and drugs that increase CNS catecholamines (Cocaine, Ephedrine, MAO inhibitors). * **Factors with NO effect on MAC:** Gender, duration of anesthesia, thyroid status, and hyper/hypokalemia.

Q: Which of the following opioid has local anesthetic properties?

Meperidine. **Explanation:** **Meperidine (Pethidine)** is unique among opioids because it possesses significant **local anesthetic properties**. This is due to its structural similarity to cocaine and its ability to block voltage-gated sodium channels, much like conventional local anesthetics (e.g., Lidocaine). When administered into the subarachnoid space, meperidine can provide both opioid-mediated analgesia and a sensory/motor block. This dual mechanism makes it the only opioid capable of being used as a sole agent for spinal anesthesia, particularly in resource-limited settings or for short procedures like saddle blocks. **Analysis of Incorrect Options:** * **Tramadol:** While it has a complex mechanism (mu-receptor agonist and reuptake inhibition of serotonin/norepinephrine), it does not possess clinically significant sodium channel blocking properties for local anesthesia. * **Fentanyl:** A potent phenylpiperidine derivative used frequently in spinal/epidural anesthesia to *augment* the block, but it lacks intrinsic local anesthetic activity and cannot produce a motor block on its own. * **Morphine:** The prototype opioid. It acts strictly via opioid receptors in the substantia gelatinosa of the spinal cord. It provides prolonged analgesia but has no effect on nerve conduction or sodium channels. **High-Yield Clinical Pearls for NEET-PG:** * **Metabolite:** Meperidine is metabolized to **normeperidine**, which is neurotoxic and can cause **seizures** (especially in renal failure). * **Side Effects:** It causes **mydriasis** (unlike the miosis seen with other opioids) due to its atropine-like structure. * **Drug Interaction:** It is strictly contraindicated with **MAO Inhibitors**, as it can precipitate a life-threatening serotonin syndrome (hyperpyrexia, coma). * **Shivers:** It is the drug of choice for treating **post-operative shivering**.

Q: Hypotension is caused by all the following anesthetic agents except:

Ketamine. **Explanation:** The correct answer is **Ketamine**. This question tests the knowledge of the hemodynamic profiles of common anesthetic agents. **1. Why Ketamine is correct:** Ketamine is a unique "dissociative" anesthetic that acts as a **sympathomimetic**. It inhibits the neuronal reuptake of catecholamines (norepinephrine), leading to an increase in heart rate, cardiac output, and arterial blood pressure. This makes it the induction agent of choice for patients in **hypovolemic or septic shock**. *Note:* While Ketamine is a direct myocardial depressant, its indirect sympathetic stimulation usually overrides this effect in healthy individuals. **2. Why the other options are incorrect:** * **Propofol:** Known for causing the most significant drop in blood pressure among induction agents. it causes profound vasodilation (decreased systemic vascular resistance) and suppresses myocardial contractility. * **Thiopentone:** A barbiturate that causes hypotension primarily through peripheral venodilation (increasing venous capacitance) and a mild direct negative inotropic effect. * **Halothane:** A volatile anesthetic that causes a dose-dependent decrease in arterial pressure, primarily by **direct myocardial depression** and interference with calcium mobilization. **Clinical Pearls for NEET-PG:** * **Agent of choice in Shock:** Ketamine. * **Agent of choice in Day-care surgery:** Propofol (due to rapid recovery). * **Agent of choice in Head Injury:** Propofol or Thiopentone (they decrease ICP). **Avoid Ketamine** as it traditionally increases ICP (though this is currently debated). * **Halothane** sensitizes the myocardium to catecholamines, increasing the risk of arrhythmias.

Q: Which drug produces a hematological side effect?

Nitrous oxide. **Explanation:** **Nitrous Oxide (N₂O)** is the correct answer because it uniquely interferes with Vitamin B12 metabolism. It irreversibly oxidizes the cobalt atom of **Vitamin B12 (cobalamin)** from the monovalent to the bivalent state. This inactivates the enzyme **methionine synthase**, which is essential for DNA synthesis. Prolonged exposure or repeated use of N₂O leads to: * **Megaloblastic Anemia:** Due to impaired DNA synthesis in the bone marrow. * **Agranulocytosis:** Reduction in white blood cell counts. * **Subacute Combined Degeneration of the Spinal Cord:** Due to impaired myelin formation. **Analysis of Incorrect Options:** * **B. Halothane:** Primarily known for its **hepatotoxicity** ("Halothane Hepatitis") and its potential to trigger Malignant Hyperthermia. It does not have significant hematological side effects. * **C. Ketamine:** Known for **dissociative anesthesia**, emergence delirium, and sympathetic stimulation (tachycardia/hypertension). It has no known effect on the hematological system. * **D. Sevoflurane:** Notable for the production of **Compound A** (nephrotoxic in rats) when reacting with soda lime and for its rapid induction/recovery. It does not cause hematological suppression. **High-Yield NEET-PG Pearls:** * **Enzyme inhibited:** Methionine Synthase. * **Test for N₂O toxicity:** Deoxyuridine suppression test (earliest indicator). * **Contraindication:** N₂O should be avoided in patients with pre-existing Vitamin B12 deficiency (e.g., Pernicious anemia, strict vegans). * **Diffusion Hypoxia:** N₂O can displace oxygen in the alveoli during recovery; always supplement with 100% O₂.

Q: If ketamine is the only agent used in reducing a dislocated shoulder, what are its actions?

Analgesia. **Explanation:** Ketamine is a unique anesthetic agent that produces **dissociative anesthesia**, characterized by a functional dissociation between the thalamocortical and limbic systems. **1. Why Analgesia is Correct:** Ketamine is a potent **NMDA receptor antagonist**. Even at sub-anesthetic doses, it provides profound **analgesia** (pain relief), making it an ideal choice for painful short procedures like reducing a dislocated shoulder. Unlike most other induction agents, it maintains protective airway reflexes and spontaneous respiration while eliminating pain. **2. Why Other Options are Incorrect:** * **Hypotension & Bradycardia (A & D):** Ketamine is a **sympathomimetic** agent. It inhibits the reuptake of catecholamines (norepinephrine), leading to an **increase** in heart rate (tachycardia) and blood pressure (hypertension). It is the induction agent of choice for patients in hemorrhagic or septic shock. * **Respiratory Depression (B):** One of ketamine’s primary advantages is that it causes **minimal respiratory depression**. It acts as a potent bronchodilator (useful in asthmatics) and generally preserves the patient's drive to breathe. **High-Yield Clinical Pearls for NEET-PG:** * **Emergence Delirium:** A common side effect characterized by hallucinations and vivid dreams; it can be prevented by co-administering **Benzodiazepines** (e.g., Midazolam). * **Secretions:** Ketamine increases salivation (sialagogue effect); **Atropine or Glycopyrrolate** is often given to counteract this. * **Contraindications:** Avoid in patients with raised Intracranial Pressure (ICP), Intraocular Pressure (IOP), or severe Ischemic Heart Disease. * **Status Asthmaticus:** Ketamine is the induction agent of choice due to its bronchodilatory properties.

Q: Which of the following is a feature of depolarizing blockade?

Progression to dual blockade. **Explanation:** Neuromuscular blockers are classified into **Depolarizing (Phase I)** and **Non-depolarizing (Phase II)** agents. Succinylcholine is the only clinically used depolarizing agent. **Why Option C is Correct:** A **Phase I (Depolarizing) block** occurs when succinylcholine mimics acetylcholine, causing persistent depolarization of the motor endplate. However, with prolonged exposure or high doses (typically >2-4 mg/kg), the block transitions into a **Phase II block (Dual Blockade)**. In this state, the membrane repolarizes but becomes desensitized to acetylcholine, clinically resembling a non-depolarizing block. **Why the other options are incorrect:** * **A & B (Tetanic fade and Post-tetanic potentiation):** These are classic features of **Non-depolarizing** blocks. In a pure Phase I depolarizing block, there is no fade; the muscle response is diminished but remains sustained (constant) during tetanic stimulation. * **D (Antagonism by anticholinesterases):** Anticholinesterases (like Neostigmine) increase acetylcholine levels. In a Phase I block, this actually **potentiates (worsens)** the blockade because it provides more substrate for depolarization. Neostigmine only antagonizes non-depolarizing blocks or a well-established Phase II block. **High-Yield NEET-PG Pearls:** * **Succinylcholine** is the drug of choice for Rapid Sequence Induction (RSI) due to its rapid onset and short duration. * **Fasciculations:** A hallmark of Phase I block, caused by the initial disorganized contraction of muscle units. * **Pseudocholinesterase:** The enzyme responsible for succinylcholine metabolism. Deficiency leads to prolonged apnea. * **Train-of-Four (TOF) Ratio:** In Phase I, the ratio is >0.7 (no fade); in Phase II/Non-depolarizing, the ratio is <0.7 (fade present).

Question 1

Which of the following statements is NOT true for propofol?

Accepted Answer

Contraindicated in porphyria

Answer

Painful intravenous administration

Answer

Induction agent

Answer

Antiemetic effect

Question 2

Abnormal plasma choline esterase produces apnea due to which of the following?

Accepted Answer

Suxamethonium

Answer

Halothane

Answer

Lignocaine

Answer

Isoflurane

Question 3

Which of the following metabolites of Atracurium is responsible for seizures?

Accepted Answer

Laudanosine

Answer

Cis-atracurium

Answer

FK-506

Answer

Gallamine

Question 4

All of the following decrease the mean alveolar concentration (MAC) of inhalational anesthetics except?

Accepted Answer

Hypothyroidism

Answer

Hypoxia

Answer

Hypercapnia

Answer

Hypovolemia

Question 5

Which of the following opioid has local anesthetic properties?

Accepted Answer

Meperidine

Answer

Tramadol

Answer

Fentanyl

Answer

Morphine

Question 6

Hypotension is caused by all the following anesthetic agents except:

Accepted Answer

Ketamine

Answer

Halothane

Answer

Propofol

Answer

Thiopentone

Question 7

Which of the following is most cardiostable?

Accepted Answer

Etomidate

Answer

Thiopentone sodium

Answer

Ketamine

Answer

Propofol

Question 8

Which drug produces a hematological side effect?

Accepted Answer

Nitrous oxide

Answer

Halothane

Answer

Ketamine

Answer

Sevoflurane

Question 9

If ketamine is the only agent used in reducing a dislocated shoulder, what are its actions?

Accepted Answer

Analgesia

Answer

Hypotension

Answer

Respiratory depression

Answer

Bradycardia

Question 10

Which of the following is a feature of depolarizing blockade?

Accepted Answer

Progression to dual blockade

Answer

Tetanic fade

Answer

Post-tetanic potentiation

Answer

Antagonism by anticholinesterases

General Anesthesia — MCQs

General Anesthesia — MCQs

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