General Anesthesia — MCQs
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Following accidental intra-arterial injection of thiopentone, what should not be done?
Which opioid drug is administered via the transdermal route?
What is a Phase I blocker?
Which of the following statements is not true about etomidate?
Which of the following is a known side effect of fentanyl?
What is commonly known as laughing gas?
Who described the stages of anesthesia?
Which of the following is NOT true about succinylcholine?
Which of the following intravenous induction agents suppresses steroidogenesis?
Ketamine should be avoided in which of the following conditions?
General Anesthesia Indian Medical PG Practice Questions and MCQs
Question 411: Following accidental intra-arterial injection of thiopentone, what should not be done?
- A. Remove the needle (Correct Answer)
- B. Intra-arterial heparin
- C. Intra-arterial papaverine
- D. Perform a stellate ganglion block
Explanation: ### Explanation The accidental intra-arterial injection of **Thiopentone** is a medical emergency. Thiopentone is highly alkaline (pH 10.5). When injected into an artery, it reacts with blood to form **crystals**, leading to intense vasospasm, chemical endarteritis, and subsequent thrombosis, which can result in gangrene. **Why "Remove the needle" is the correct answer:** The most critical rule in managing intra-arterial thiopentone is to **leave the needle in situ**. Removing the needle loses the only direct access to the affected vessel. The needle should be kept in place to serve as a conduit for administering emergency vasodilators and anticoagulants directly to the site of the spasm. **Analysis of other options (Management steps):** * **Intra-arterial Papaverine:** This is a potent vasodilator used to counteract the intense arterial spasm. It should be injected through the indwelling needle. * **Intra-arterial Heparin:** Used to prevent the formation of thrombi around the thiopentone crystals and damaged endothelium. * **Stellate Ganglion Block:** This provides sympathetic blockade, leading to reflex vasodilation of the upper limb vessels, thereby improving collateral circulation. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of injury:** Crystal formation and norepinephrine release leading to vasospasm. * **Clinical presentation:** Immediate, intense "burning" pain distal to the site of injection and loss of distal pulses. * **Other management steps:** * Dilute the drug by injecting Normal Saline. * Lidocaine (1%) for vasodilation and pain relief. * Brachial plexus block (alternative to Stellate block). * **Gold Standard:** Leave the needle in place!
Question 412: Which opioid drug is administered via the transdermal route?
- A. Sulfentanil
- B. Remifentanil
- C. Fentanyl (Correct Answer)
- D. Alfentanil
Explanation: **Explanation:** **Fentanyl** is the correct answer because it possesses the ideal physicochemical properties for transdermal delivery: high lipid solubility, low molecular weight, and high potency. The **Fentanyl Transdermal Patch** (Durogesic) utilizes a rate-limiting membrane to provide stable plasma concentrations over 72 hours. It is primarily used for chronic cancer pain and is not suitable for acute or postoperative pain due to its slow onset (12–24 hours to reach peak effect) and long offset. **Analysis of Incorrect Options:** * **A. Sufentanil:** While highly potent and lipid-soluble, it is primarily used intravenously or via the sublingual route (Zalviso) for acute pain. Transdermal formulations exist but are not standard clinical practice compared to Fentanyl. * **B. Remifentanil:** This drug is unique due to its metabolism by **non-specific plasma esterases**, giving it an ultra-short duration of action (half-life <10 mins). It must be given via continuous IV infusion; a transdermal route would defeat the purpose of its rapid titratability. * **C. Alfentanil:** It has a rapid onset and short duration, used mainly for blunting the pressor response to intubation. It is less lipid-soluble than Fentanyl, making it less suitable for transdermal application. **High-Yield Clinical Pearls for NEET-PG:** * **Potency Ratio:** Sufentanil (1000x) > Fentanyl (100x) > Morphine (1x). * **Context-Sensitive Half-Time:** Remifentanil remains constant regardless of infusion duration, whereas Fentanyl increases significantly after long infusions. * **Fentanyl Patch Caution:** Fever or external heat (e.g., heating pads) can increase drug release from the patch, leading to potential overdose/respiratory depression.
Question 413: What is a Phase I blocker?
- A. Depolarization blockade (Correct Answer)
- B. Desensitization blockade
- C. Both
- D. Neither
Explanation: **Explanation:** Neuromuscular blocking agents are classified into two main categories based on their mechanism of action at the nicotinic acetylcholine receptors (nAChR) of the motor endplate: **Depolarizing** and **Non-depolarizing** agents. **Why Option A is Correct:** Succinylcholine (Suxamethonium) is the only clinically used depolarizing muscle relaxant. It acts as an agonist at the nAChR, causing prolonged stimulation. This leads to an initial depolarization of the motor endplate (clinically seen as **fasciculations**), followed by a persistent state where the membrane cannot repolarize to receive further impulses. This initial mechanism is termed a **Phase I Blockade**. Key characteristics include the absence of "fade" on Train-of-Four (TOF) stimulation and the absence of post-tetanic facilitation. **Why Other Options are Incorrect:** * **Option B (Desensitization blockade):** This is synonymous with a **Phase II Blockade**. It occurs after prolonged exposure or high doses of Succinylcholine. The membrane eventually repolarizes but becomes "desensitized" and unresponsive to acetylcholine, behaving like a non-depolarizing block (showing "fade" on TOF). * **Option C & D:** These are incorrect as Phase I is specifically defined by the initial depolarization event. **NEET-PG High-Yield Pearls:** * **Metabolism:** Succinylcholine is rapidly metabolized by **Pseudocholinesterase** (Plasma cholinesterase). * **Side Effects:** Hyperkalemia (avoid in burns/trauma), bradycardia (especially in children), and it is a potent trigger for **Malignant Hyperthermia**. * **Anticholinesterases:** Giving Neostigmine during a Phase I block will **prolong** the paralysis rather than reverse it, as it increases the concentration of acetylcholine at the junction.
Question 414: Which of the following statements is not true about etomidate?
- A. It is an intravenous anesthetic.
- B. It precipitates coronary insufficiency. (Correct Answer)
- C. It inhibits cortisol synthesis.
- D. It causes pain at the site of injection.
Explanation: **Explanation:** Etomidate is a carboxylated imidazole derivative used for the induction of general anesthesia. The correct answer is **B** because Etomidate is renowned for its **hemodynamic stability**. It has minimal effects on heart rate, stroke volume, and cardiac output, making it the induction agent of choice for patients with cardiac disease or hypovolemia. It does **not** precipitate coronary insufficiency; in fact, it maintains coronary perfusion pressure. **Analysis of Options:** * **Option A (True):** Etomidate is a potent, short-acting **intravenous** induction agent that acts via the GABA-A receptor complex. * **Option C (True):** This is a classic side effect. Etomidate causes dose-dependent **adrenocortical suppression** by inhibiting the enzyme **11-beta-hydroxylase**, which is essential for cortisol and aldosterone synthesis. This effect can last for 6–24 hours after a single dose. * **Option D (True):** Due to its formulation in propylene glycol, Etomidate frequently causes **pain on injection** and is associated with a high incidence of postoperative nausea and vomiting (PONV) and myoclonus. **High-Yield NEET-PG Pearls:** 1. **Drug of Choice:** For induction in patients with **cardiovascular instability**, shock, or limited cardiac reserve. 2. **Myoclonus:** Common during induction; can be minimized by premedication with opioids or benzodiazepines. 3. **Cerebral Effects:** It decreases Cerebral Metabolic Rate (CMRO2), Cerebral Blood Flow (CBF), and Intraocular Pressure (IOP). 4. **Avoidance:** Should be used cautiously in septic patients due to its inhibitory effect on the stress response (cortisol suppression).
Question 415: Which of the following is a known side effect of fentanyl?
- A. Abdominal pain
- B. Hypertension
- C. Tachycardia
- D. Chest wall rigidity (Correct Answer)
Explanation: **Explanation:** **Chest wall rigidity** (also known as "Wooden Chest Syndrome") is a classic and high-yield side effect of potent synthetic opioids like **fentanyl, sufentanil, and remifentanil**. This phenomenon occurs due to the rapid intravenous administration of high doses, leading to intense contraction of the thoracic and abdominal muscles via the activation of mu-opioid receptors in the central nervous system. This rigidity can make bag-mask ventilation nearly impossible, requiring immediate management with neuromuscular blocking agents (like succinylcholine) or opioid antagonists (naloxone). **Analysis of Incorrect Options:** * **Abdominal pain:** Opioids generally provide visceral analgesia. While they can cause biliary colic due to the spasm of the Sphincter of Oddi, generalized abdominal pain is not a characteristic acute side effect. * **Hypertension & Tachycardia:** Fentanyl is known for its **hemodynamic stability**. It typically causes a decrease in sympathetic outflow, often leading to **hypotension and bradycardia** (via central vagal stimulation), rather than elevation of blood pressure or heart rate. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Rigidity:** It is thought to be mediated by the inhibition of GABA release or stimulation of dopaminergic pathways in the basal ganglia. * **Prevention:** Administer fentanyl slowly and in titrated doses. * **Context:** Fentanyl is 100 times more potent than morphine and is preferred in cardiac anesthesia due to its lack of histamine release (unlike morphine). * **Miosis:** Like most opioids, fentanyl causes "pin-point pupils" due to stimulation of the Edinger-Westphal nucleus.
Question 416: What is commonly known as laughing gas?
- A. Ketamine
- B. Nitric oxide
- C. Nitrous oxide (Correct Answer)
- D. Methane
Explanation: **Explanation:** **Nitrous oxide ($N_2O$)** is a colorless, odorless gas widely known as **"laughing gas"** because it often induces a state of euphoria, giddiness, and involuntary laughter upon inhalation. In clinical practice, it is a weak anesthetic but a potent analgesic. It is the only inorganic gas used in modern anesthesia and is typically administered in combination with oxygen and volatile anesthetics to achieve the "Second Gas Effect." **Analysis of Incorrect Options:** * **Ketamine (Option A):** Known as a "dissociative anesthetic," it produces a trance-like state. It is often referred to as "Special K" in recreational contexts, but not laughing gas. * **Nitric oxide (Option B):** This is $NO$, a potent endogenous vasodilator used clinically to treat pulmonary hypertension. It is chemically distinct from Nitrous oxide ($N_2O$) and does not have anesthetic properties. * **Methane (Option D):** A hydrocarbon gas ($CH_4$) that is flammable and not used in clinical anesthesia. **High-Yield Clinical Pearls for NEET-PG:** * **MAC Value:** Nitrous oxide has a very high Minimum Alveolar Concentration (MAC) of **104%**, making it impossible to produce surgical anesthesia alone at atmospheric pressure. * **Blood-Gas Partition Coefficient:** It has a low coefficient (**0.47**), leading to rapid induction and recovery. * **Diffusion Hypoxia:** Post-operatively, $N_2O$ rapidly diffuses from the blood into the alveoli, diluting oxygen. This is prevented by administering **100% oxygen** for 5–10 minutes after turning off the gas. * **Contraindications:** It should be avoided in conditions where air is trapped in closed body cavities (e.g., pneumothorax, intestinal obstruction, middle ear surgery, or air embolism) because it expands these spaces. * **Vitamin B12:** Chronic exposure can lead to megaloblastic anemia and peripheral neuropathy by inactivating methionine synthase.
Question 417: Who described the stages of anesthesia?
- A. WTG Moon
- B. Oliver Wendell Holmes
- C. John Snow
- D. Guedel (Correct Answer)
Explanation: **Explanation:** The correct answer is **D. Guedel**. **Arthur Ernest Guedel** described the four stages of anesthesia in 1920, primarily based on the clinical signs observed during the administration of **Diethyl Ether** (a slow-acting inhalational agent) in spontaneously breathing patients. These stages were crucial for monitoring depth before the advent of modern monitoring and neuromuscular blockers. * **Stage I (Analgesia):** From induction to loss of consciousness. * **Stage II (Excitement/Delirium):** Characterized by irregular breathing, struggling, and risk of laryngospasm. * **Stage III (Surgical Anesthesia):** Divided into 4 planes; characterized by regular breathing and loss of reflexes. * **Stage IV (Medullary Paralysis/Overdose):** Respiratory and vasomotor collapse (to be avoided). **Why other options are incorrect:** * **WTG Morton (Option A):** Often confused with "Moon," William T.G. Morton gave the first successful public demonstration of ether anesthesia in 1846 at the "Ether Dome." * **Oliver Wendell Holmes (Option B):** A physician and poet who coined the term **"Anesthesia"** (meaning "without sensation"). * **John Snow (Option C):** Considered the first specialist anesthetist; he famously administered chloroform to Queen Victoria and is also the father of modern epidemiology. **High-Yield Clinical Pearls for NEET-PG:** * **Guedel’s signs** are best seen with **Ether**. They are obscured by modern rapid-acting IV agents (like Propofol) and muscle relaxants. * **Stage II** is the most dangerous stage (risk of vomiting and laryngospasm). * **Guedel’s Airway:** An oropharyngeal airway named after him, used to maintain patency in unconscious patients.
Question 418: Which of the following is NOT true about succinylcholine?
- A. Causes fasciculations
- B. Increases intracranial pressure
- C. It is a non-depolarizing neuromuscular blocker (Correct Answer)
- D. It is a short-acting muscle relaxant
Explanation: **Explanation:** Succinylcholine (Suxamethonium) is the only **depolarizing neuromuscular blocker** used clinically. It works by mimicking acetylcholine at the nicotinic receptors of the motor endplate, causing prolonged depolarization which renders the muscle fiber unresponsive to further stimulation. Therefore, Option C is incorrect (and the right answer) because succinylcholine is **not** a non-depolarizing agent (like Vecuronium or Atracurium). **Analysis of other options:** * **Option A (Fasciculations):** Before causing paralysis, succinylcholine triggers disorganized muscle contractions known as fasciculations. This is a hallmark of depolarizing blockers. * **Option B (Increased Intracranial Pressure):** Succinylcholine is known to transiently increase ICP, likely due to fasciculations and increased afferent muscle spindle activity. It should be used with caution in patients with head injuries. * **Option D (Short-acting):** It has the fastest onset (30–60 seconds) and shortest duration of action (5–10 minutes) because it is rapidly hydrolyzed by **pseudocholinesterase** (butyrylcholinesterase) in the plasma. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** For Rapid Sequence Induction (RSI) due to its rapid onset and offset. * **Side Effects:** Hyperkalemia (avoid in burns, trauma, or denervation injuries), myalgia, and increased intraocular/intragastric pressure. * **Malignant Hyperthermia:** Succinylcholine is a potent trigger for Malignant Hyperthermia (Treatment: Dantrolene). * **Phase II Block:** Occurs with repeated doses or infusions, where the block starts behaving like a non-depolarizing block. * **Dibucaine Number:** Used to test for atypical pseudocholinesterase; a low number (e.g., 20) indicates a genetic deficiency leading to prolonged apnea.
Question 419: Which of the following intravenous induction agents suppresses steroidogenesis?
- A. Thiopentone
- B. Ketamine
- C. Propofol
- D. Etomidate (Correct Answer)
Explanation: **Explanation:** **Correct Answer: D. Etomidate** Etomidate is a carboxylated imidazole derivative used for intravenous induction. Its most significant side effect is the **dose-dependent inhibition of the enzyme 11-beta-hydroxylase**. This enzyme is essential for converting 11-deoxycortisol to cortisol and 11-deoxycorticosterone to aldosterone in the adrenal cortex. Even a single induction dose can suppress adrenal steroidogenesis for 6 to 24 hours, which may be detrimental in patients with sepsis or adrenal insufficiency. **Analysis of Incorrect Options:** * **A. Thiopentone:** A short-acting barbiturate that acts via GABA-A receptors. Its primary side effects are cardiovascular and respiratory depression; it does not interfere with the adrenal axis. * **B. Ketamine:** A NMDA receptor antagonist. It is unique because it causes sympathetic stimulation (increasing BP and HR) and has no inhibitory effect on steroid synthesis. * **C. Propofol:** An isopropylphenol that enhances GABAergic neurotransmission. While it causes significant vasodilation and hypotension, it does not affect the endocrine function of the adrenal gland. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Etomidate is the induction agent of choice for patients with **hemodynamic instability** (e.g., shock, severe cardiac disease) because it has minimal effects on heart rate and blood pressure. * **Myoclonus:** Etomidate is frequently associated with excitatory movements (myoclonus) during induction, which can be prevented by premedication with opioids or benzodiazepines. * **Porphyria:** Like barbiturates, Etomidate should be avoided in patients with acute intermittent porphyria as it can induce ALA synthetase. * **Nausea/Vomiting:** It has a higher incidence of Postoperative Nausea and Vomiting (PONV) compared to propofol.
Question 420: Ketamine should be avoided in which of the following conditions?
- A. Increased arterial pressure (Correct Answer)
- B. Pregnancy
- C. Hypovolemic shock
- D. Asthma
Explanation: **Explanation:** Ketamine is a unique dissociative anesthetic agent that acts primarily as an **NMDA receptor antagonist**. Unlike most other induction agents, it stimulates the sympathetic nervous system, leading to a "sympathomimetic effect." **1. Why Option A is Correct:** Ketamine causes an indirect stimulation of the cardiovascular system by inhibiting the reuptake of catecholamines (norepinephrine). This results in an **increase in heart rate, cardiac output, and arterial blood pressure**. Therefore, it is strictly contraindicated in patients with pre-existing hypertension, ischemic heart disease, or increased intracranial pressure, as it can exacerbate these conditions. **2. Why Incorrect Options are Wrong:** * **B. Pregnancy:** Ketamine is not contraindicated in pregnancy. In fact, it is often used in obstetric emergencies (like placental abruption) due to its ability to maintain blood pressure. It does not affect uterine blood flow significantly at standard doses. * **C. Hypovolemic Shock:** Ketamine is the **induction agent of choice** for patients in hemorrhagic or hypovolemic shock. Its sympathomimetic properties help maintain hemodynamic stability when other agents (like propofol) would cause dangerous hypotension. * **D. Asthma:** Ketamine is the **induction agent of choice** for patients with reactive airway disease/asthma. It has potent **bronchodilatory** effects due to catecholamine release. **High-Yield Clinical Pearls for NEET-PG:** * **Dissociative Anesthesia:** Characterized by eyes remaining open with a slow nystagmic gaze (catalepsy). * **Emergence Delirium:** A common side effect (hallucinations/vivid dreams), which can be pre-treated with **Benzodiazepines** (Midazolam). * **Secretions:** Ketamine increases salivation; **Glycopyrrolate** is often co-administered to prevent this. * **Reflexes:** Pharyngeal and laryngeal reflexes are usually maintained, but the risk of aspiration still exists.
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
Practice Questions
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