NEET-PG 2012 — Anesthesiology

Q: Which of the following is true about coeliac plexus block?

Most common side effects include diarrhea and hypotension. ***Most common side effects include diarrhea and hypotension*** - A coeliac plexus block interrupts **sympathetic innervation** to the upper abdominal organs, which can lead to parasympathetic dominance. - This imbalance often results in **increased gastrointestinal motility (diarrhea)** and **vasodilation (hypotension)** as common side effects. *Located retroperitoneally at the level of L3* - The coeliac plexus is typically located **retroperitoneally** at the level of the **T12-L1 vertebrae**, not L3. - Its position is generally superior to the renal arteries, which are closer to L1-L2. *Usually done unilaterally* - A coeliac plexus block is almost always performed **bilaterally** or with a single posterior approach aiming for bilateral spread to effectively block the plexus. - The coeliac plexus is an extensive network, and a unilateral block would likely provide inadequate pain relief. *Useful for painful conditions of the lower abdomen* - The coeliac plexus primarily innervates **upper abdominal organs** (e.g., pancreas, liver, stomach, small intestine, kidneys, adrenal glands). - It is therefore generally **ineffective for lower abdominal pain**, which is innervated by different sympathetic plexuses (e.g., superior and inferior hypogastric plexuses). [Practice more Anesthesiology PYQs on OnCourse]

Q: What is the potential respiratory complication associated with the use of Trilene in combination with Sodalime?

Airway irritation and inflammation. ***Airway irritation and inflammation*** - The interaction between **Trilene (trichloroethylene)** and **soda lime** in a closed anesthetic circuit can produce **dichloroacetylene**. - **Dichloroacetylene** is a highly toxic compound that can cause severe airway irritation, inflammation, and even **necrosis** of the respiratory tract. *Renal toxicity* - While some halogenated anesthetics (e.g., methoxyflurane) are associated with **renal toxicity** due to fluoride ion release, this is not the primary or most severe respiratory complication of Trilene with soda lime. - The main concern with Trilene and soda lime is the formation of a **toxic airway irritant**. *Hepatotoxicity* - **Halothane** is more classically associated with **hepatotoxicity** (halothane hepatitis) due to metabolism into toxic intermediates. - **Trilene** itself is not primarily known for causing severe hepatotoxicity, and the interaction with soda lime does not specifically target the liver for toxicity. *Myocardial depression* - Many inhaled anesthetics, including Trilene, can cause some degree of **myocardial depression**. - However, this is a general effect of the anesthetic on cardiac function and is not a unique or specific complication arising from the **interaction with soda lime** that produces dichloroacetylene. [Practice more Anesthesiology PYQs on OnCourse]

Q: Calcium homeostasis disturbance is the predominant pathophysiological mechanism in

Malignant hyperthermia. ***Malignant hyperthermia*** - Malignant hyperthermia is caused by a genetic defect in the **ryanodine receptor (RYR1)** in skeletal muscle, leading to an uncontrolled release of **intracellular calcium** from the sarcoplasmic reticulum. - This excessive calcium release results in sustained muscle contraction, increased metabolism, and a rapid rise in body temperature. *Duchenne Muscular Dystrophy (DMD)* - DMD is primarily caused by a mutation in the **dystrophin gene**, which leads to the absence or severe deficiency of the **dystrophin protein**. - This deficiency results in muscle fiber fragility, cycles of degeneration and regeneration, and eventual replacement of muscle with fibrous and fatty tissue, rather than a primary calcium homeostasis disturbance. *Limb Girdle Muscular Dystrophy* - This group of disorders is characterized by progressive weakness and wasting of muscles, primarily affecting the **shoulders and hips**. - The pathophysiology involves genetic defects in various proteins that are crucial for muscle function and integrity, such as **sarcoglycans** or **calpain-3**, not primarily calcium dysregulation. *Tibial Muscular Dystrophy* - Tibial muscular dystrophy is a rare, late-onset disorder characterized by progressive weakness of the **anterior tibial muscles**. - It is typically caused by mutations in the **TTN gene**, encoding for the protein **titin**, which plays a vital role in muscle elasticity and structural integrity, rather than a primary calcium imbalance. [Practice more Anesthesiology PYQs on OnCourse]

Q: Who is known for demonstrating the levels of ether anesthesia?

Guedel. ***Guedel*** - Arthur Guedel developed and refined the **stages and planes of ether anesthesia** based on clinical observations of respiratory patterns, eye signs, and muscle tone. - His classification system, known as the **Guedel stages**, provided a systematic approach to monitoring anesthetic depth, especially useful before the advent of modern anesthetic agents and monitoring equipment. *Morton* - **William T.G. Morton** is credited with the first successful public demonstration of sulfuric ether as a surgical anesthetic in 1846 during a tooth extraction. - While he pioneered the use of ether for anesthesia, he did not develop the classic stages of anesthetic depth. *Thompson* - There is no widely recognized historical figure named Thompson who is primarily known for defining the **levels or stages of ether anesthesia**. - This name is not associated with the primary discovery or classification of anesthetic depth. *None of the options* - This option is incorrect because **Guedel** is specifically known for his work in defining the stages of ether anesthesia. - Guedel's contributions were significant in standardizing anesthetic practice for many years. [Practice more Anesthesiology PYQs on OnCourse]

Q: What does the Dibucaine number indicate in clinical practice?

Atypical acetylcholinesterase activity. ***Atypical acetylcholinesterase activity*** - The **Dibucaine number** quantifies the inhibition of **pseudocholinesterase (butyrylcholinesterase)** by the local anesthetic dibucaine. - A low Dibucaine number (e.g., < 20-30) indicates a genetically determined **atypical variant** of pseudocholinesterase, leading to prolonged duration of action of drugs like succinylcholine. *Potency of muscle relaxants* - The potency of muscle relaxants is typically assessed by the **ED95**, which is the dose required to produce 95% suppression of twitch response. - While Dibucaine is a local anesthetic that can cause muscle relaxation, the **Dibucaine number** specifically evaluates an enzyme's activity, not the strength of the relaxant itself. *Potency of general anesthetics* - The potency of general anesthetics is primarily measured by the **Minimum Alveolar Concentration (MAC)** required to prevent movement in 50% of patients in response to a noxious stimulus. - The Dibucaine number is unrelated to the mechanism or potency of general anesthetic agents. *None of the options* - This option is incorrect because **Atypical acetylcholinesterase activity** accurately describes what the Dibucaine number indicates. - The Dibucaine number is a specific laboratory test used to identify genetic variations in butyrylcholinesterase, which has significant clinical implications for drug metabolism. [Practice more Anesthesiology PYQs on OnCourse]

20 Previous Year Questions with Answers & Explanations

Questions

Which of the following is true about coeliac plexus block?

What is the potential respiratory complication associated with the use of Trilene in combination with Sodalime?

Calcium homeostasis disturbance is the predominant pathophysiological mechanism in

Who is known for demonstrating the levels of ether anesthesia?

What does the Dibucaine number indicate in clinical practice?

All of the following cause myocardial depression except:

Cocaine was first used as a local anesthetic by?

What is the critical temperature of Nitrous Oxide (N2O)?

Which of the following statements about halothane is false?

Q10

Ayre's T-piece is which type of circuit

NEET-PG 2012 - Anesthesiology NEET-PG Practice Questions and MCQs

Question 1: Which of the following is true about coeliac plexus block?

A. Usually done unilaterally
B. Most common side effects include diarrhea and hypotension (Correct Answer)
C. Located retroperitoneally at the level of L3
D. Useful for painful conditions of the lower abdomen

Explanation: ***Most common side effects include diarrhea and hypotension*** - A coeliac plexus block interrupts **sympathetic innervation** to the upper abdominal organs, which can lead to parasympathetic dominance. - This imbalance often results in **increased gastrointestinal motility (diarrhea)** and **vasodilation (hypotension)** as common side effects. *Located retroperitoneally at the level of L3* - The coeliac plexus is typically located **retroperitoneally** at the level of the **T12-L1 vertebrae**, not L3. - Its position is generally superior to the renal arteries, which are closer to L1-L2. *Usually done unilaterally* - A coeliac plexus block is almost always performed **bilaterally** or with a single posterior approach aiming for bilateral spread to effectively block the plexus. - The coeliac plexus is an extensive network, and a unilateral block would likely provide inadequate pain relief. *Useful for painful conditions of the lower abdomen* - The coeliac plexus primarily innervates **upper abdominal organs** (e.g., pancreas, liver, stomach, small intestine, kidneys, adrenal glands). - It is therefore generally **ineffective for lower abdominal pain**, which is innervated by different sympathetic plexuses (e.g., superior and inferior hypogastric plexuses).

Question 2: What is the potential respiratory complication associated with the use of Trilene in combination with Sodalime?

A. Renal toxicity
B. Hepatotoxicity
C. Myocardial depression
D. Airway irritation and inflammation (Correct Answer)

Explanation: ***Airway irritation and inflammation*** - The interaction between **Trilene (trichloroethylene)** and **soda lime** in a closed anesthetic circuit can produce **dichloroacetylene**. - **Dichloroacetylene** is a highly toxic compound that can cause severe airway irritation, inflammation, and even **necrosis** of the respiratory tract. *Renal toxicity* - While some halogenated anesthetics (e.g., methoxyflurane) are associated with **renal toxicity** due to fluoride ion release, this is not the primary or most severe respiratory complication of Trilene with soda lime. - The main concern with Trilene and soda lime is the formation of a **toxic airway irritant**. *Hepatotoxicity* - **Halothane** is more classically associated with **hepatotoxicity** (halothane hepatitis) due to metabolism into toxic intermediates. - **Trilene** itself is not primarily known for causing severe hepatotoxicity, and the interaction with soda lime does not specifically target the liver for toxicity. *Myocardial depression* - Many inhaled anesthetics, including Trilene, can cause some degree of **myocardial depression**. - However, this is a general effect of the anesthetic on cardiac function and is not a unique or specific complication arising from the **interaction with soda lime** that produces dichloroacetylene.

Question 3: Calcium homeostasis disturbance is the predominant pathophysiological mechanism in

A. Duchenne Muscular Dystrophy (DMD)
B. Limb Girdle Muscular Dystrophy
C. Malignant hyperthermia (Correct Answer)
D. Tibial Muscular Dystrophy

Explanation: ***Malignant hyperthermia*** - Malignant hyperthermia is caused by a genetic defect in the **ryanodine receptor (RYR1)** in skeletal muscle, leading to an uncontrolled release of **intracellular calcium** from the sarcoplasmic reticulum. - This excessive calcium release results in sustained muscle contraction, increased metabolism, and a rapid rise in body temperature. *Duchenne Muscular Dystrophy (DMD)* - DMD is primarily caused by a mutation in the **dystrophin gene**, which leads to the absence or severe deficiency of the **dystrophin protein**. - This deficiency results in muscle fiber fragility, cycles of degeneration and regeneration, and eventual replacement of muscle with fibrous and fatty tissue, rather than a primary calcium homeostasis disturbance. *Limb Girdle Muscular Dystrophy* - This group of disorders is characterized by progressive weakness and wasting of muscles, primarily affecting the **shoulders and hips**. - The pathophysiology involves genetic defects in various proteins that are crucial for muscle function and integrity, such as **sarcoglycans** or **calpain-3**, not primarily calcium dysregulation. *Tibial Muscular Dystrophy* - Tibial muscular dystrophy is a rare, late-onset disorder characterized by progressive weakness of the **anterior tibial muscles**. - It is typically caused by mutations in the **TTN gene**, encoding for the protein **titin**, which plays a vital role in muscle elasticity and structural integrity, rather than a primary calcium imbalance.

Question 4: Who is known for demonstrating the levels of ether anesthesia?

A. Morton
B. Guedel (Correct Answer)
C. Thompson
D. None of the options

Explanation: ***Guedel*** - Arthur Guedel developed and refined the **stages and planes of ether anesthesia** based on clinical observations of respiratory patterns, eye signs, and muscle tone. - His classification system, known as the **Guedel stages**, provided a systematic approach to monitoring anesthetic depth, especially useful before the advent of modern anesthetic agents and monitoring equipment. *Morton* - **William T.G. Morton** is credited with the first successful public demonstration of sulfuric ether as a surgical anesthetic in 1846 during a tooth extraction. - While he pioneered the use of ether for anesthesia, he did not develop the classic stages of anesthetic depth. *Thompson* - There is no widely recognized historical figure named Thompson who is primarily known for defining the **levels or stages of ether anesthesia**. - This name is not associated with the primary discovery or classification of anesthetic depth. *None of the options* - This option is incorrect because **Guedel** is specifically known for his work in defining the stages of ether anesthesia. - Guedel's contributions were significant in standardizing anesthetic practice for many years.

Question 5: What does the Dibucaine number indicate in clinical practice?

A. Atypical acetylcholinesterase activity (Correct Answer)
B. Potency of muscle relaxants
C. Potency of general anesthetics
D. None of the options

Explanation: ***Atypical acetylcholinesterase activity*** - The **Dibucaine number** quantifies the inhibition of **pseudocholinesterase (butyrylcholinesterase)** by the local anesthetic dibucaine. - A low Dibucaine number (e.g., < 20-30) indicates a genetically determined **atypical variant** of pseudocholinesterase, leading to prolonged duration of action of drugs like succinylcholine. *Potency of muscle relaxants* - The potency of muscle relaxants is typically assessed by the **ED95**, which is the dose required to produce 95% suppression of twitch response. - While Dibucaine is a local anesthetic that can cause muscle relaxation, the **Dibucaine number** specifically evaluates an enzyme's activity, not the strength of the relaxant itself. *Potency of general anesthetics* - The potency of general anesthetics is primarily measured by the **Minimum Alveolar Concentration (MAC)** required to prevent movement in 50% of patients in response to a noxious stimulus. - The Dibucaine number is unrelated to the mechanism or potency of general anesthetic agents. *None of the options* - This option is incorrect because **Atypical acetylcholinesterase activity** accurately describes what the Dibucaine number indicates. - The Dibucaine number is a specific laboratory test used to identify genetic variations in butyrylcholinesterase, which has significant clinical implications for drug metabolism.

Question 6: All of the following cause myocardial depression except:

A. Halothane
B. Thiopentone
C. Etomidate (Correct Answer)
D. Ketamine

Explanation: ***Etomidate*** - **Etomidate** is known for its **hemodynamic stability** and minimal effect on myocardial contractility, making it a suitable induction agent for patients with cardiovascular compromise. - While it can cause some decrease in systemic vascular resistance, it maintains **cardiac output** much better than other agents listed. *Halothane* - **Halothane** is a potent volatile anesthetic that directly depresses **myocardial contractility** and reduces cardiac output. - It sensitizes the myocardium to **catecholamines**, increasing the risk of arrhythmias. *Thiopentone* - **Thiopentone** (thiopental) is a barbiturate that causes significant **dose-dependent myocardial depression** and systemic vasodilation. - This can lead to a substantial decrease in **blood pressure** and cardiac output, especially with rapid administration. *Ketamine* - Although ketamine often causes an increase in heart rate and blood pressure due to **sympathetic stimulation**, it can also have a direct **myocardial depressant effect** when the sympathetic nervous system is exhausted or blocked. - Its indirect stimulant effects *can mask* a direct negative inotropic effect on the myocardium.

Question 7: Cocaine was first used as a local anesthetic by?

A. Holmer Wells
B. Morton
C. Carl Koller (Correct Answer)
D. None of the options

Explanation: ***Carl Koller*** - **Carl Koller** (1857-1944), an Austrian ophthalmologist, is credited with the first clinical use of cocaine as a local anesthetic in 1884. - He demonstrated its efficacy for topical anesthesia in eye surgery, revolutionizing surgical practices. *Holmer Wells* - **Horace Wells** (not Holmer) was an American dentist who pioneered the use of **nitrous oxide** as an anesthetic in dentistry in the 1840s, preceding Koller's work with cocaine. - His contributions were focused on general anesthesia for pain relief during tooth extractions. *Morton* - **William T.G. Morton** was another American dentist who famously demonstrated the use of **ether** as a surgical anesthetic in 1846. - His work popularized surgical anesthesia, but it was not related to cocaine as a local anesthetic. *None of the options* - This option is incorrect because Carl Koller is historically recognized as the pioneer for the clinical use of **cocaine as a local anesthetic**.

Question 8: What is the critical temperature of Nitrous Oxide (N2O)?

A. -118°C
B. -36°C
C. -30°C
D. -36.5°C (Correct Answer)

Explanation: **-36.5°C** - The **critical temperature** of **nitrous oxide (N2O)** is **36.5°C**, which is the temperature above which it cannot be liquefied by pressure alone. - This value is important for understanding the **physical state** and safe handling of N2O, as deviations can lead to phase changes or storage issues. *-118°C* - This temperature is significantly lower than the actual critical temperature of N2O and is incorrect. - This value might be related to the **boiling point of other gases** but not the critical temperature of N2O. *-36°C* - While close, **-36°C** is not the precise critical temperature for nitrous oxide. - This small difference can be significant in contexts requiring **exact physical properties** of gases. *-30°C* - This temperature is incorrect and is higher than the actual critical temperature of N2O. - At this temperature, N2O would still behave as a **liquefiable gas** under sufficient pressure, indicating it is below its critical point.

Question 9: Which of the following statements about halothane is false?

A. Volatile liquid with sweet odour
B. Constricts bronchii (Correct Answer)
C. Causes malignant hyperthermia
D. Sensitises heart to adrenaline

Explanation: ***Constricts bronchii*** - Halothane is a **bronchodilator** that relaxes bronchial smooth muscle, making it useful in patients with asthma or COPD. - The statement that it constricts bronchi is **false**. *Volatile liquid with sweet odour* - **Halothane** is a **volatile liquid** and is known for its characteristic **sweet, non-pungent odour**. - This property makes it well-tolerated during induction of anesthesia, particularly in pediatric patients. *Sensitises heart to adrenaline* - Halothane **sensitizes the myocardium** to the effects of **catecholamines**, including adrenaline (epinephrine). - This can lead to the development of **cardiac arrhythmias**, especially ventricular arrhythmias, when adrenaline is administered or endogenous levels are high. *Causes malignant hyperthermia* - Halothane is a potent trigger for **malignant hyperthermia**, a rare but life-threatening pharmacogenetic disorder. - This condition is characterized by a rapid and severe increase in body temperature, muscle rigidity, and metabolic derangements due to uncontrolled release of calcium from the sarcoplasmic reticulum.

Question 10: Ayre's T-piece is which type of circuit

A. Type A
B. Type B
C. Type E (Correct Answer)
D. Type D

Explanation: ***Type E*** - The **Ayre's T-piece** is classified as a **Type E breathing circuit** according to the classification of Mapleson circuits. - It is a modification of the Mapleson A circuit, widely used in pediatric anesthesia due to its high efficiency and low resistance. *Type A* - **Mapleson A circuits** have the fresh gas flow (FGF) inlet near the patient and a reservoir bag at the circuit's most distal end. - While very efficient for spontaneous ventilation, they are not the same as an Ayre's T-piece. *Type B* - **Mapleson B circuits** have the fresh gas flow inlet and the reservoir bag near the patient, with the expiratory valve further away. - This configuration is generally inefficient for both spontaneous and controlled ventilation. *Type D* - **Mapleson D circuits** have the fresh gas flow inlet near the patient and the expiratory valve close to the reservoir bag, which is distal to the patient. - These circuits are commonly used for controlled ventilation, but are not the Ayre's T-piece.