General Anesthesia Practice Questions

Q: A patient on atracurium develops seizures due to accumulation of

Laudanosine. ***Laudanosine*** - **Laudanosine** is a metabolite of atracurium which is known to cross the **blood-brain barrier** and can cause **seizures** and central nervous system excitation, especially in high concentrations or in patients with impaired renal or hepatic function. - Atracurium undergoes **Hofmann elimination** and **ester hydrolysis** to produce laudanosine and other inactive metabolites. *Sulfated Atracurium* - **Atracurium** is not primarily metabolized through sulfation; its primary degradation pathways are **Hofmann elimination** and **ester hydrolysis**. - There is no known direct association between sulfated atracurium and seizure activity. *Hofmann elimination products* - **Hofmann elimination** is one of the main pathways for atracurium degradation, but the *overall products* are numerous, and **laudanosine** is the specific metabolite implicated in seizures. - While laudanosine is a product of Hofmann elimination, this option is too broad and does not pinpoint the neurotoxic metabolite. *Ester hydrolysis products* - **Ester hydrolysis** is another significant pathway for atracurium metabolism, but, similar to Hofmann elimination, it produces various metabolites. - **Laudanosine** is formed via Hofmann elimination; ester hydrolysis primarily produces quaternary acid and alcohol products, which are not directly linked to seizure activity.

Q: Which muscle is most resistant to neuromuscular blockage?

Diaphragm. ***Diaphragm*** - The **diaphragm** is functionally resistant to neuromuscular blocking agents due to its high density of acetylcholine receptors and different isoform of nicotinic receptors. - Due to its vital role in respiration, it is the last muscle to be paralyzed and the first to recover from neuromuscular blockade. *Adductor pollicis* - The **adductor pollicis** is a commonly used muscle for monitoring neuromuscular blockade as it is highly sensitive to the effects of these agents. - Its response correlates well with the blockade of muscles in the **larynx and pharynx**, making it a good indicator for intubation conditions. *Ocular* - **Ocular muscles** are among the first muscles to be affected by neuromuscular blockers. - They tend to show partial recovery while other muscles are still significantly blocked, reflecting their high metabolic rate and sparse acetylcholine receptor distribution. *Intercostal muscles* - **Intercostal muscles** are accessory muscles of respiration that are more sensitive to neuromuscular blockade than the diaphragm. - They are paralyzed relatively early in the process and recover later than the diaphragm, leading to reduced tidal volume even when the diaphragm is functional.

Q: Nephrotoxic anaesthetic agent is :

Methoxyflurane. ***Methoxyflurane*** - **Methoxyflurane** is metabolized to inorganic fluoride ions, which can cause dose-dependent **nephrotoxicity** by damaging renal tubules and impairing the kidneys' concentrating ability. - Due to its significant risk of kidney damage, **methoxyflurane** is now rarely used as an anesthetic in clinical practice, though it is still used as an inhaled analgesic in some regions. *Isoflurane* - **Isoflurane** has a low metabolic rate and is largely excreted unchanged, making its potential for organ toxicity, including **nephrotoxicity**, much lower compared to methoxyflurane. - It is considered a relatively safe and commonly used inhalational anesthetic for cardiovascular stability and minimal renal effects. *Halothane* - **Halothane** is primarily associated with **hepatotoxicity** (halothane hepatitis) due to its metabolism into reactive intermediates, rather than nephrotoxicity. - While it can cause some degree of renal vasoconstriction, its direct toxic effects on the kidneys are not a primary concern compared to its hepatic risks. *Nitrous Oxide* - **Nitrous oxide** has minimal direct organ toxicity, including to the kidneys, as it is largely eliminated unchanged via the lungs. - Its main concern is its potential to inactivate **vitamin B12**, which can lead to megaloblastic anemia and neurological deficits with prolonged exposure.

Q: Which of the following anesthetic drugs is contraindicated in chronic renal failure?

Pethidine. ***Pethidine*** - **Pethidine** is contraindicated in chronic renal failure due to its active metabolite, **normeperidine**, which is eliminated renally. - Accumulation of **normeperidine** can lead to **central nervous system (CNS) toxicity**, including seizures, tremors, and hyperreflexia. *Atracurium* - **Atracurium** undergoes **Hofmann elimination** and **ester hydrolysis**, which are independent of renal or hepatic function. - This makes it a relatively safe choice for patients with **renal impairment**. *Fentanyl* - **Fentanyl** is primarily metabolized by the liver, with its metabolites being inactive. - While some dose adjustment may be considered in severe renal failure, it is generally **safe** for use in patients with chronic renal impairment as its metabolites are inactive. *Morphine* - **Morphine** is metabolized in the liver to **morphine-3-glucuronide (M3G)** and **morphine-6-glucuronide (M6G)**, both of which are renally excreted. - **M6G** is an active metabolite with potent analgesic effects, and its accumulation in renal failure can cause **prolonged sedation** and **respiratory depression**. While significant caution and dose reduction are needed, it's not strictly contraindicated in the same way pethidine is due to the more neurotoxic nature of normeperidine.

Q: Diffusion hypoxia is seen with –

Nitrous oxide. ***Nitrous oxide*** - **Diffusion hypoxia** occurs when **nitrous oxide** rapidly diffuses out of the blood and into the alveoli during elimination, diluting the partial pressures of oxygen and carbon dioxide. - This rapid diffusion can lead to a transient decrease in the **partial pressure of oxygen** in the alveoli, potentially causing hypoxia if patients are not given supplemental oxygen during recovery. *Cyclopropane* - **Cyclopropane** is an older, potent inhalational anesthetic not commonly used today due to its **flammability** and high risk of **cardiac arrhythmias**. - It does not cause diffusion hypoxia as its blood solubility and elimination characteristics differ significantly from nitrous oxide. *Halothane* - **Halothane** is a potent volatile anesthetic that can cause **dose-dependent myocardial depression** and **hepatotoxicity**. - Its elimination primarily occurs via the lungs, but its relatively high blood solubility and slower wash-out prevent the rapid alveolar gas dilution seen with nitrous oxide, thus not causing diffusion hypoxia. *Ether* - **Ether** (**diethyl ether**) is another historical anesthetic agent known for its strong analgesic properties and slow induction/recovery. - While it has a high blood-gas solubility, its slower kinetics of elimination do not lead to the rapid outward diffusion phenomenon that causes diffusion hypoxia.

Q: Which of the following anaesthetic agent lacks analgesic effect? A) N2O B) Thiopentone C) Methohexitone D) Ketamine E) Fentanyl

Thiopentone. ***Thiopentone*** - Thiopentone is a **barbiturate** anesthetic primarily used for inducing anesthesia. - It provides significant **hypnosis** and sedation but lacks intrinsic **analgesic properties**, meaning it does not relieve pain. *N2O* - **Nitrous oxide** (N2O) is an inhalation anesthetic that provides good **analgesia** at sub-anesthetic concentrations. - It is often used as an adjunct to other anesthetic agents to enhance pain relief during procedures. *Methohexitone* - Methohexitone is another **barbiturate** similar to thiopentone, used for induction of anesthesia. - While it provides rapid **hypnosis**, it also lacks significant **analgesic effects**. *Ketamine* - Ketamine is a **dissociative anesthetic** known for its potent **analgesic properties**. - It works by blocking **NMDA receptors**, providing pain relief even at sub-anesthetic doses. *Fentanyl* - Fentanyl is a powerful **opioid analgesic** that is commonly used in anesthesia for its strong pain-relieving effects. - It acts on **opioid receptors** in the central nervous system to reduce pain perception.

Q: Risk of adverse effects of SCOLINE is greater in

Spinal cord injury. ***Spinal cord injury*** - Patients with **spinal cord injury** are at increased risk of developing **hyperkalemia** due to upregulation of extrajunctional acetylcholine receptors, which can be life-threatening after administration of **succinylcholine (Scoline)**. - This risk is highest in the period **7 days to several months post-injury**, making succinylcholine relatively contraindicated during this time. *Thoracic injury* - While thoracic injuries can be severe, they **do not directly lead to the widespread upregulation of extrajunctional acetylcholine receptors** that cause succinylcholine-induced hyperkalemia. - The primary concerns with succinylcholine in thoracic injury relate to its effects on **respiratory drive** or potential for **increased intrathoracic pressure**, but not extreme hyperkalemia. *Head injury* - Patients with head injuries may require rapid sequence intubation, and succinylcholine is often used, but it does **not inherently carry a higher risk of hyperkalemia** due to receptor upregulation. - The main concern with succinylcholine in head injury is a potential, albeit controversial, for a **transient increase in intracranial pressure**, which is different from hyperkalemia. *Bone injury* - **Isolated bone injuries**, even severe ones, do not cause the same profound muscle denervation or immobility that leads to the upregulation of extrajunctional acetylcholine receptors seen in spinal cord injury. - Therefore, the risk of **succinylcholine-induced hyperkalemia** is not significantly elevated in patients with only bone injuries.

Q: When using low-flow circle absorber techniques, the uptake of nitrous oxide must be considered. In a healthy 70 kg adult, the expected uptake of nitrous oxide, with a 70% inspired concentration, after 1.5 hours would be about

100 ml/min. ***100 ml/min*** - The uptake of **nitrous oxide (N2O)** decreases significantly over time as the blood and tissue compartments become saturated. After 1.5 hours, the uptake slows considerably. - At this point, the uptake rate for a 70 kg adult with 70% N2O is expected to be approximately **100 ml/min**, reflecting the near-saturation of less vascular tissues. *500 ml/min* - An uptake of **500 ml/min** is typical during the **initial, rapid uptake phase** of nitrous oxide (first 5-15 minutes) as it quickly equilibrates with the blood and highly perfused tissues. - This rate would be too high after 1.5 hours, as the body's capacity to absorb N2O has decreased significantly. *250 ml/min* - This rate represents an **intermediate phase** of N2O uptake, typically occurring within the first 30-60 minutes, when the drug is still being absorbed into moderately perfused tissues. - After 1.5 hours, the uptake would have slowed down further than this rate due to continued saturation of tissue compartments. *1000 ml/min* - An uptake of **1000 ml/min** (or 1 L/min) is an **extremely high rate** of N2O uptake, far exceeding what is physiologically possible in a 70 kg adult even during the initial rapid phase. - This would imply a massive, unsustainable absorption, which is not clinically relevant for N2O in a healthy individual.

Q: Competitive neuromuscular blockade is enhanced by all except

Hypercalcemia. ***Hypercalcemia*** - **Hypercalcemia** generally **antagonizes** the effects of neuromuscular blockers by increasing acetylcholine release at the presynaptic terminal and sensitizing the postsynaptic membrane to acetylcholine. - Therefore, it would **reduce**, rather than enhance, competitive neuromuscular blockade. *Acidosis* - **Acidosis** enhances competitive neuromuscular blockade by altering the sensitivity of the **nicotinic acetylcholine receptors** at the neuromuscular junction. - It also affects the pharmacokinetics and pharmacodynamics of neuromuscular blocking agents, leading to **prolonged blockade**. *Aminoglycosides* - **Aminoglycoside antibiotics** like gentamicin or amikacin can enhance neuromuscular blockade by **inhibiting presynaptic acetylcholine release** and blocking postsynaptic nicotinic receptors. - This effect is particularly pronounced when given concurrently with competitive neuromuscular blocking agents. *Hypermagnesemia* - **Hypermagnesemia** enhances neuromuscular blockade by **decreasing acetylcholine release** from the presynaptic nerve terminal. - It also directly **depresses muscle fiber excitability** and reduces the sensitivity of the postsynaptic membrane to acetylcholine.

Q: Which of the following intravenous anesthetic agents is contraindicated in epileptic patients posted for general anaesthesia

Ketamine. ***Ketamine*** - Ketamine is known to have **proconvulsant effects**, particularly at higher doses, and can exacerbate seizures in epileptic patients. - It causes **dissociative anesthesia** and can increase intracranial pressure, which is generally undesirable in patients with seizure disorders. *Thiopentone* - Thiopentone is a **barbiturate** that acts as an anticonvulsant and is often used to treat seizures or status epilepticus, making it safe in epileptic patients. - It **decreases cerebral metabolic rate** and intracranial pressure, which are beneficial for patients with neurologic conditions. *Midazolam* - Midazolam is a **benzodiazepine** with strong anticonvulsant properties, frequently used to terminate seizures. - It enhances GABAergic inhibition, making it a **safe and effective sedative** for epileptic patients. *Propofol* - Propofol has **anticonvulsant properties** and is often used in the management of refractory status epilepticus. - It **decreases cerebral blood flow** and metabolic rate, making it a favorable choice in patients with epilepsy.

Question 1

A patient on atracurium develops seizures due to accumulation of

Accepted Answer

Laudanosine

Answer

Sulfated Atracurium

Answer

Hofmann elimination products

Answer

Ester hydrolysis products

Question 2

Which muscle is most resistant to neuromuscular blockage?

Accepted Answer

Diaphragm

Answer

Adductor pollicis

Answer

Ocular

Answer

Intercostal muscles

Question 3

Nephrotoxic anaesthetic agent is :

Accepted Answer

Methoxyflurane

Answer

Isoflurane

Answer

Halothane

Answer

Nitrous Oxide

Question 4

Which of the following anesthetic drugs is contraindicated in chronic renal failure?

Accepted Answer

Pethidine

Answer

Atracurium

Answer

Fentanyl

Answer

Morphine

Question 5

Diffusion hypoxia is seen with –

Accepted Answer

Nitrous oxide

Answer

Cyclopropane

Answer

Halothane

Answer

Ether

Question 6

Which of the following anaesthetic agent lacks analgesic effect?

A) N2O
B) Thiopentone  
C) Methohexitone
D) Ketamine
E) Fentanyl

Accepted Answer

Thiopentone

Answer

N2O

Answer

Methohexitone

Answer

Ketamine

Answer

Fentanyl

Question 7

Risk of adverse effects of SCOLINE is greater in

Accepted Answer

Spinal cord injury

Answer

Thoracic injury

Answer

Head injury

Answer

Bone injury

Question 8

When using low-flow circle absorber techniques, the uptake of nitrous oxide must be considered. In a healthy 70 kg adult, the expected uptake of nitrous oxide, with a 70% inspired concentration, after 1.5 hours would be about

Accepted Answer

100 ml/min

Answer

500 ml/min

Answer

250 ml/min

Answer

1000 ml/min

Question 9

Competitive neuromuscular blockade is enhanced by all except

Accepted Answer

Hypercalcemia

Answer

Acidosis

Answer

Aminoglycosides

Answer

Hypermagnesemia

Question 10

Which of the following intravenous anesthetic agents is contraindicated in epileptic patients posted for general anaesthesia

Accepted Answer

Ketamine

Answer

Thiopentone

Answer

Midazolam

Answer

Propofol

General Anesthesia — MCQs

General Anesthesia — MCQs

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