General Anesthesia Practice Questions

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

Suxamethonium (Sch). **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.

Q: Which of the following statements about sugammadex is true?

It selectively binds to rocuronium.. **Explanation:** **1. Why the Correct Answer is Right:** Sugammadex is a **selective relaxant binding agent (SRBA)**. It is a modified gamma-cyclodextrin molecule designed with a lipophilic core and a hydrophilic exterior. Its mechanism of action involves encapsulating the aminosteroid neuromuscular blocking agent (NMBA) molecule in a 1:1 ratio, creating a guest-host complex. This effectively lowers the free plasma concentration of the drug, causing it to diffuse away from the nicotinic acetylcholine receptors at the neuromuscular junction. It has the highest affinity for **rocuronium**, followed by vecuronium. **2. Why the Other Options are Wrong:** * **Option A:** Sugammadex only works on **aminosteroid** NMBAs. Succinylcholine is a depolarizing NMBA (a benzylisocholine derivative) and is metabolized by pseudocholinesterase; sugammadex has no effect on it. * **Option C:** Sugammadex is a **reversal agent** used at the *end* of surgery or for emergency rescue. It is not used for the *induction* of anesthesia itself, though it allows for the safe use of high-dose rocuronium in Rapid Sequence Induction (RSI) by providing a "fail-safe" for rapid reversal. * **Option D:** Atracurium and Cisatracurium are **benzylisoquinolinium** compounds. Their molecular structure does not fit into the sugammadex cyclodextrin ring; therefore, they cannot be reversed by it. **3. Clinical Pearls for NEET-PG:** * **Dosing:** 2 mg/kg for routine reversal (TOF count ≥2); 4 mg/kg for deep blockade (PTC 1-2); 16 mg/kg for immediate rescue reversal after 1.2 mg/kg rocuronium. * **Side Effects:** Anaphylaxis (rare but significant) and transient bradycardia. * **Drug Interaction:** It can bind to oral contraceptives, rendering them ineffective; patients should be advised to use alternative contraception for 7 days post-administration. * **Elimination:** The sugammadex-rocuronium complex is excreted unchanged by the **kidneys**.

Q: Which of the following intravenous induction agents suppresses steroidogenesis?

Etomidate. **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.

Q: Regarding suxamethonium, all are true except?

It is recommended in patients with burns.. **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).

Q: Which of the following anesthetic agents can be safely used in a patient with asthma?

Ketamine. **Explanation:** The primary goal in the anesthetic management of an asthmatic patient is to avoid bronchospasm and provide bronchodilation. **Why Ketamine is the Correct Answer:** Ketamine is the induction agent of choice for patients with asthma or reactive airway disease. It possesses potent **bronchodilatory properties** mediated through two mechanisms: 1. **Sympathomimetic effect:** It increases the release of endogenous catecholamines, which stimulate $\beta_2$ receptors. 2. **Direct smooth muscle relaxation:** It has a direct relaxant effect on the bronchial smooth muscle. Additionally, it maintains functional residual capacity (FRC) and does not typically suppress the respiratory drive as significantly as other agents. **Analysis of Incorrect Options:** * **Thiopentone:** It is generally **contraindicated** in asthma. It can cause histamine release and may lead to life-threatening bronchospasm, especially if the airway is manipulated during light planes of anesthesia. * **Etomidate:** While hemodynamically stable, it has no bronchodilatory properties. It is also associated with myoclonus and adrenocortical suppression. * **Propofol:** While Propofol is actually a good choice for asthmatics (it is a bronchodilator and suppresses airway reflexes), **Ketamine is superior** in an acute setting or for patients with active wheezing due to its active sympathomimetic bronchodilation. In many MCQ formats, Ketamine is the "most correct" classical answer. **High-Yield NEET-PG Pearls:** * **Drug of Choice for Induction in Asthma:** Ketamine. * **Inhalational Agent of Choice:** Sevoflurane (least pungent, potent bronchodilator). * **Avoid:** Desflurane (pungent, can cause airway irritation) and Morphine (histamine release). * **Pre-medication:** Glycopyrrolate is preferred over Atropine to reduce secretions without causing significant tachycardia.

Q: Which anesthetic agent is known to dissolve rubber?

Halothane. **Explanation:** **Halothane** is a halogenated hydrocarbon that acts as a potent organic solvent. It is uniquely known for its ability to dissolve or degrade **rubber and certain plastics**. This occurs because halothane molecules can penetrate the polymer chains of natural rubber, causing it to swell, lose elasticity, and eventually disintegrate. This property necessitated the development of specialized "antistatic" neoprene or plastic components in anesthetic breathing circuits and vaporizers to prevent equipment failure. **Analysis of Incorrect Options:** * **Enflurane (B):** While it is a halogenated ether, it is much less corrosive than halothane and does not significantly degrade rubber components used in modern clinical practice. * **Cyclopropane (C):** This is an explosive gas. While it requires specific precautions regarding static electricity and rubber (to prevent sparks), it does not chemically dissolve the rubber itself. * **Ether (D):** Diethyl ether is highly flammable and can cause rubber to swell slightly over prolonged exposure, but it lacks the potent solvent action seen with halothane. **High-Yield Clinical Pearls for NEET-PG:** * **Corrosion:** Halothane also corrodes metals like aluminum, brass, and lead, especially in the presence of moisture. * **Preservative:** Because halothane is unstable, it is stored in amber-colored bottles with **0.01% Thymol** added as a stabilizing agent to prevent spontaneous decomposition. * **Vaporizer:** Halothane requires a **variable bypass, agent-specific vaporizer** (e.g., Fluotec) because of its specific saturated vapor pressure. * **Hepatotoxicity:** Remember the "Halothane Hepatitis" association, often linked to the formation of trifluoroacetylated liver proteins.

Q: Which side effect of halothane is countered by atropine?

Bradycardia. **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.

Q: Which anesthetic agent is least metabolized in the body?

Xenon. **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.

Q: What effect does ketamine produce?

Analgesia. **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).

Question 1

Phase II block is seen in which of the following?

Accepted Answer

Suxamethonium (Sch)

Answer

d-Tubocurarine (d-TC)

Answer

Ether

Answer

Nitrous Oxide (N2O)

Question 2

Which of the following statements about sugammadex is true?

Accepted Answer

It selectively binds to rocuronium.

Answer

It antagonizes succinylcholine.

Answer

It is used with rocuronium for rapid induction of anesthesia.

Answer

It reverses the effects of atracurium.

Question 3

Which of the following intravenous induction agents suppresses steroidogenesis?

Accepted Answer

Etomidate

Answer

Thiopentone

Answer

Propofol

Answer

Ketamine

Question 4

Regarding suxamethonium, all are true except?

Accepted Answer

It is recommended in patients with burns.

Answer

It is metabolized principally by plasma cholinesterase.

Answer

It should be used cautiously in patients using echothiopate eye drops for glaucoma.

Answer

It can cause hyperkalemia.

Question 5

Which of the following anesthetic agents can be safely used in a patient with asthma?

Accepted Answer

Ketamine

Answer

Thiopentone

Answer

Etomidate

Answer

Propofol

Question 6

Which anesthetic agent is known to dissolve rubber?

Accepted Answer

Halothane

Answer

Enflurane

Answer

Cyclopropane

Answer

Ether

Question 7

Which side effect of halothane is countered by atropine?

Accepted Answer

Bradycardia

Answer

Hypotension

Answer

Hyperthermia

Answer

Constipation

Question 8

Which anesthetic agent is least metabolized in the body?

Accepted Answer

Xenon

Answer

Ether

Answer

Halothane

Answer

Methoxyflurane

Question 9

What effect does ketamine produce?

Accepted Answer

Analgesia

Answer

Allodynia

Answer

Hyperpathia

Answer

Dystonia

Question 10

Regarding suxamethonium-induced apnea, all are true except:

Accepted Answer

It is due to a deficiency of cholinesterase.

Answer

It is caused by suxamethonium.

Answer

It can be inherited.

Answer

Mortality is very low in recent times with proper management.

General Anesthesia — MCQs

General Anesthesia — MCQs

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