General Anesthesia Practice Questions

Q: Which of the following intravenous agents is commonly used for outpatient procedures?

Propofol. ***Propofol*** - It is the **drug of choice** for outpatient anesthesia due to its **rapid onset** and short duration of action, allowing for a **rapid recovery** profile. - It possesses **anti-emetic properties** and provides clear-headed recovery, making it ideal for **day-case surgery**. *Ketamine* - It is a **dissociative anesthetic** associated with **post-operative emergence delirium** and hallucinations in adults. - While useful in emergency or pediatric settings, it causes **increased salivation** and **increased intracranial/intraocular pressure**, limiting its routine outpatient use. *Thiopental* - An ultrashort-acting **barbiturate** that was historically used for induction but has a long redistribution phase, leading to a **prolonged hang-over effect**. - Its use is largely obsolete in outpatient settings due to **cardiovascular depression** and a slower recovery compared to newer agents. *Etomidate* - Known for cardiovascular stability, but it causes **adrenocortical suppression** with prolonged infusion, making it less suitable for anything beyond single-dose induction. - Frequently associated with **post-operative nausea and vomiting (PONV)** and **myoclonus**, which can interfere with the immediate post-operative experience in a day-care setting.

Q: A 40-year-old female is scheduled for parotid surgery and is administered general Anaesthesia. Approximately 10 minutes into the procedure, the following findings are noted: - Rise in end-tidal CO2 (EtCO2) - Temperature: 104°F (40°C) - Heart rate: 150 bpm - Blood pressure: 180/110 mmHg What is the most likely diagnosis?

Malignant hyperthermia. ***Malignant hyperthermia*** - This is a pharmacogenetic disorder triggered by volatile inhalational anesthetics or succinylcholine, characterized by a hypermetabolic state. - The rapid rise in **end-tidal CO2 (EtCO2)** is often the earliest sign, followed by **tachycardia**, severe **hyperthermia**, and **hypertension** due to muscle rigidity. *Heat stroke* - Typically caused by environmental exposure or extreme physical exertion, not triggered by anesthetic agents. - Patients often present with altered mental status and dry skin, occurring much later and not immediately following induction. *Heat cramps* - This is a mild form of heat illness characterized by painful muscle spasms caused by salt and water depletion. - It does not present with the systemic hypermetabolic crisis seen here, such as the rapid rise in **EtCO2** or life-threatening tachycardia. *Heat pyrexia* - Also known as heat exhaustion, this condition involves systemic symptoms like dizziness and fatigue due to heat stress. - It lacks the acute, life-threatening hypermetabolic surge associated with anesthesia administration.

Q: A 34-year-old asthmatic male undergoes elective laparoscopic cholecystectomy under general anesthesia with endotracheal intubation. Fifteen minutes after induction, the ventilator alarm sounds for high peak airway pressure. The anesthesiologist notes the waveform shown on the capnograph monitor (Image 1). What is the most likely cause of this capnographic pattern?

A. Severe bronchospasm causing expiratory flow obstruction. ***A. Severe bronchospasm causing expiratory flow obstruction*** - The classic **"shark-fin"** appearance on capnography (sloping Phase II and upward-slanting Phase III) indicates **expiratory flow obstruction** where alveoli empty asynchronously. - In an **asthmatic** patient, this pattern combined with **increased peak airway pressures** is highly diagnostic of acute bronchospasm during general anesthesia. *B. Esophageal intubation with absent alveolar gas exchange* - **Esophageal intubation** typically results in a complete **absence of CO2** or a few rapidly decreasing small waves as stomach gas is depleted. - It does not produce the sustained, characteristic waveform morphology associated with **obstructive lung disease**. *C. Pulmonary embolism causing increased alveolar dead space* - **Pulmonary embolism** increases **alveolar dead space**, which typically causes a sharp **decrease in End-Tidal CO2 (EtCO2)** levels. - The waveform morphology remains relatively normal, rather than showing the **obstructive upswing** seen in bronchospasm. *D. Malignant hyperthermia causing increased CO2 production* - **Malignant hyperthermia** presents with a rapid, massive **increase in EtCO2** due to hypermetabolism. - While total CO2 levels rise significantly, the **plateau phase (Phase III)** of the capnogram usually remains flat unless secondary airway issues occur.

Q: Diffusion hypoxia is seen with which drug?

Nitrous oxide. **Explanation:** **Nitrous Oxide (N₂O)** is the correct answer because of its unique pharmacokinetic property: high solubility in blood compared to nitrogen, but low overall solubility compared to other anesthetics. **The Mechanism (Fink Effect):** Diffusion hypoxia occurs during the **recovery phase** of anesthesia. When N₂O administration is stopped, it rushes out of the blood and into the alveoli down its concentration gradient. Because N₂O is 30 times more soluble than nitrogen, it floods the alveoli in massive volumes. This "dilutes" the alveolar oxygen and carbon dioxide. The resulting drop in alveolar oxygen tension ($PAO_2$) leads to arterial hypoxemia. To prevent this, clinicians administer **100% oxygen for 5–10 minutes** after discontinuing N₂O. **Analysis of Incorrect Options:** * **Ketamine:** An intravenous NMDA receptor antagonist. It does not involve alveolar gas exchange mechanisms and is known for maintaining airway reflexes and respiratory drive. * **Theophylline:** A methylxanthine used as a bronchodilator in asthma/COPD. It is not an anesthetic gas and does not cause diffusion hypoxia. * **Halothane:** A volatile inhalational anesthetic. While it can cause respiratory depression, it does not diffuse in large enough volumes to dilute alveolar oxygen significantly. **High-Yield NEET-PG Pearls:** * **Second Gas Effect:** N₂O speeds up the induction of a companion volatile anesthetic (e.g., Halothane) by creating a "vacuum" in the alveoli as it is rapidly absorbed. * **Concentration Effect:** The higher the concentration of N₂O inhaled, the more rapidly the arterial concentration rises. * **Contraindication:** N₂O should be avoided in closed-space pathologies (e.g., pneumothorax, intestinal obstruction, middle ear surgery) because it expands air-filled cavities.

Q: All of the following are modes to decrease pain on injection caused by propofol except?

Use vein on the dorsum of hand. **Explanation:** Propofol is a highly lipophilic drug, but its aqueous phase contains free propofol molecules that irritate the venous intima and activate the **kallikrein-kinin system**, leading to significant pain on injection. **Why Option C is the Correct Answer (The "Except"):** Using a vein on the **dorsum of the hand** actually **increases** the incidence and severity of pain compared to larger, more proximal veins. For NEET-PG, remember that the gold standard for reducing propofol-induced pain is using a **large-bore cannula in a large vein** (e.g., the antecubital fossa), which allows for faster dilution of the drug and less contact with the vessel wall. **Analysis of Other Options:** * **A. Mix Lignocaine with Propofol:** This is the most common clinical practice. Lignocaine (10–40 mg) acts as a local anesthetic on the vein wall and stabilizes the kinin cascade. * **B. Give Fentanyl prior to Propofol:** Pre-treatment with opioids like Fentanyl or Alfentanil increases the pain threshold and provides central analgesia, effectively reducing the injection pain. * **D. Cooling of the Drug:** Cooling propofol to 4°C reduces the concentration of free propofol in the aqueous phase and slows down the activation of pain mediators. **High-Yield Clinical Pearls for NEET-PG:** * **Propofol Formulation:** It is an emulsion (1% propofol, 10% soybean oil, 2.25% glycerol, and 1.2% egg phosphatide). * **Other methods to reduce pain:** Using Long-Chain Triglyceride/Medium-Chain Triglyceride (LCT/MCT) emulsions or the **Bier’s Block technique** (applying a tourniquet before injecting lignocaine). * **Contraindication:** Avoid propofol in patients with a documented severe allergy to **egg yolk** (though most egg allergies are to the albumin in the white).

Q: Which of the following statements about nitrous oxide is FALSE?

It is a good muscle relaxant.. **Explanation:** Nitrous oxide ($N_2O$) is a commonly used inhalational anesthetic agent, but it possesses specific pharmacological properties that make Option D the false statement. **Why Option D is Correct (The False Statement):** Nitrous oxide is a potent analgesic but a very weak anesthetic (MAC = 104%). Crucially, it has **no muscle relaxant properties**. In clinical practice, it must be supplemented with neuromuscular blocking agents or more potent volatile anesthetics (like Isoflurane) to achieve the surgical relaxation required for abdominal or thoracic procedures. **Analysis of Other Options:** * **Option A:** It is historically and commonly referred to as **"laughing gas"** due to the euphoric effects it produces upon inhalation. * **Option B:** $N_2O$ oxidizes the cobalt atom in **Vitamin B12**, inactivating methionine synthase. Prolonged exposure or chronic abuse leads to impaired DNA synthesis, resulting in **megaloblastic anemia** and subacute combined degeneration of the spinal cord. * **Option C:** Due to its low blood-gas solubility, $N_2O$ exits the blood into the alveoli rapidly once discontinued. This dilutes the alveolar oxygen concentration, leading to **diffusion hypoxia** (Fink effect). This is prevented by administering 100% oxygen for 5–10 minutes after stopping $N_2O$. **High-Yield NEET-PG Pearls:** * **Second Gas Effect:** $N_2O$ accelerates the uptake of a companion volatile anesthetic. * **Closed Spaces:** $N_2O$ is 34 times more soluble than Nitrogen; it diffuses into air-filled cavities faster than nitrogen can leave, increasing volume/pressure. It is **contraindicated** in pneumothorax, intestinal obstruction, air embolism, and middle ear surgeries. * **Concentration Effect:** The higher the concentration inhaled, the more rapid the induction.

Q: Which of the following drugs are known to be hepatotoxic?

Both chloroform and halothane. **Explanation:** The correct answer is **C (Both chloroform and halothane)** because both agents are historically and clinically associated with significant hepatotoxicity through different mechanisms. **1. Chloroform:** It is a potent hepatotoxin. Its toxicity is primarily due to its metabolism by cytochrome P450 into **phosgene**, a highly reactive metabolite. This causes direct centrilobular hepatic necrosis, leading to its withdrawal from clinical practice. **2. Halothane:** It is notorious for causing **"Halothane Hepatitis."** This occurs via two mechanisms: * **Type I (Minor):** A self-limiting, transient rise in transaminases. * **Type II (Major):** A rare but severe immune-mediated reaction. Halothane is metabolized to trifluoroacetyl chloride, which binds to hepatic proteins to form **haptens**. This triggers an antibody response, leading to massive hepatic necrosis. **Why other options are incorrect:** * **Option A & B:** These are partially correct but incomplete, as both drugs share the property of being hepatotoxic. * **Option D:** This is incorrect because both drugs have well-documented histories of causing liver injury. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors for Halothane Hepatitis:** Multiple exposures (most important), obesity, female gender, and middle age. * **Metabolism:** Halothane is the most metabolized volatile anesthetic (~20%), which contributes to its toxicity. * **Safest Profile:** **Sevoflurane and Desflurane** are the least metabolized and are not associated with immune-mediated hepatitis. * **Rule of Thumb:** In a patient with pre-existing liver disease or previous halothane exposure, avoid halothane; use Isoflurane (the "gold standard" for liver surgery due to maintained hepatic blood flow).

Q: Non-depolarizing neuromuscular blockade is potentiated by which of the following conditions or medications?

Quinidine. **Explanation:** The potentiation of non-depolarizing neuromuscular blockers (NDNMBs) is a high-yield topic in anesthesia. **Quinidine** (Option D) potentiates NDNMBs by decreasing the release of acetylcholine from the pre-junctional nerve terminal and reducing the sensitivity of the post-junctional nicotinic receptors. It also exerts a direct depressant effect on the muscle membrane. **Analysis of Options:** * **Quinidine (Correct):** Class IA antiarrhythmics (like quinidine and procainamide) and other drugs like calcium channel blockers, aminoglycosides, and local anesthetics significantly prolong the duration of neuromuscular blockade. * **Hyperkalemia (Incorrect):** High potassium levels partially depolarize the muscle membrane, making it *more* excitable. This actually **antagonizes** (resists) the effects of NDNMBs. Conversely, **hypokalemia** potentiates NDNMBs. * **Hypomagnesemia (Incorrect):** Magnesium inhibits calcium entry into the pre-junctional terminal, reducing ACh release. Therefore, **hypermagnesemia** (not hypo) potentiates NDNMBs. * **Chronic Phenytoin Therapy (Incorrect):** Chronic use of anticonvulsants (phenytoin, carbamazepine) leads to **resistance** to NDNMBs due to the up-regulation of acetylcholine receptors. However, an *acute* dose of phenytoin may potentiate the block. **High-Yield Clinical Pearls for NEET-PG:** 1. **Electrolytes that Potentiate NDNMBs:** Hypokalemia, Hypermagnesemia, Hypocalcemia, and Respiratory Acidosis. 2. **Antibiotics that Potentiate NDNMBs:** Aminoglycosides (Neomycin > Streptomycin > Amikacin) are the most potent. 3. **Temperature:** Hypothermia prolongs the block by slowing metabolism and excretion (especially for Atracurium/Vecuronium). 4. **Lithium:** Potentiates both depolarizing (Succinycholine) and non-depolarizing blockers.

Q: A 35-year-old patient is given excessive intravenous Benzodiazepine. She suddenly becomes agitated, combative, and exhibits involuntary movements. The anesthesiologist determines that she is having a reaction to the drug which has been given in excess. What is the next step in management?

Flumazenil. ### Explanation **Correct Answer: B. Flumazenil** **Mechanism and Rationale:** The patient is experiencing a **paradoxical reaction** to benzodiazepines (BZDs). While BZDs are typically used for sedation and anxiolysis, excessive doses or specific patient factors can trigger agitation, combativeness, and involuntary movements. **Flumazenil** is a specific **competitive antagonist** at the benzodiazepine receptor site on the GABA-A receptor complex. It rapidly reverses both the sedative effects and the paradoxical reactions caused by BZDs. In clinical practice, it is the "gold standard" antidote for BZD overdose or to reverse deep sedation postoperatively. **Analysis of Incorrect Options:** * **A. Protamine:** This is the specific antagonist used to reverse the anticoagulant effects of **Heparin**. It has no role in managing sedative toxicity. * **C. Buprenorphine:** A partial opioid agonist-antagonist used primarily for pain management or opioid de-addiction. It would not reverse BZD-induced symptoms. * **D. Morphine:** An opioid agonist. Giving morphine to an already agitated or over-sedated patient could worsen respiratory depression and complicate the clinical picture. **High-Yield Clinical Pearls for NEET-PG:** * **Half-life Caution:** Flumazenil has a shorter half-life (approx. 1 hour) than most benzodiazepines (e.g., Diazepam). **Resedation** can occur, so the patient must be monitored closely for several hours. * **Contraindication:** Avoid Flumazenil in patients with a history of **seizures** or those on long-term BZDs, as it can precipitate acute withdrawal seizures. * **Dosage:** The initial recommended dose is 0.2 mg IV over 15 seconds, repeated as necessary up to 1 mg. * **Paradoxical Reactions:** These are more common in pediatric and geriatric populations, or those with psychiatric comorbidities.

Question 1

Which of the following intravenous agents is commonly used for outpatient procedures?

Accepted Answer

Propofol

Answer

Ketamine

Answer

Thiopental

Answer

Etomidate

Question 2

A 40-year-old female is scheduled for parotid surgery and is administered general Anaesthesia.
Approximately 10 minutes into the procedure, the following findings are noted:
- Rise in end-tidal CO2 (EtCO2)
- Temperature: 104°F (40°C)
- Heart rate: 150 bpm
- Blood pressure: 180/110 mmHg
What is the most likely diagnosis?

Accepted Answer

Malignant hyperthermia

Answer

Heat stroke

Answer

Heat cramps

Answer

Heat pyrexia

Question 3

A 34-year-old asthmatic male undergoes elective laparoscopic cholecystectomy under general anesthesia with endotracheal intubation. Fifteen minutes after induction, the ventilator alarm sounds for high peak airway pressure. The anesthesiologist notes the waveform shown on the capnograph monitor (Image 1). What is the most likely cause of this capnographic pattern?

Accepted Answer

A. Severe bronchospasm causing expiratory flow obstruction

Answer

B. Esophageal intubation with absent alveolar gas exchange

Answer

C. Pulmonary embolism causing increased alveolar dead space

Answer

D. Malignant hyperthermia causing increased CO2 production

Question 4

Diffusion hypoxia is seen with which drug?

Accepted Answer

Nitrous oxide

Answer

Ketamine

Answer

Theophylline

Answer

Halothane

Question 5

All of the following are modes to decrease pain on injection caused by propofol except?

Accepted Answer

Use vein on the dorsum of hand

Answer

Mix lignocaine with propofol

Answer

Give fentanyl prior to propofol

Answer

Cooling of the drug

Question 6

Which of the following statements about nitrous oxide is FALSE?

Accepted Answer

It is a good muscle relaxant.

Answer

It is also known as laughing gas.

Answer

It can cause megaloblastic anemia.

Answer

It can lead to diffusion hypoxia.

Question 7

Which of the following drugs are known to be hepatotoxic?

Accepted Answer

Both chloroform and halothane

Answer

Chloroform

Answer

Halothane

Answer

Neither chloroform nor halothane

Question 8

Non-depolarizing neuromuscular blockade is potentiated by which of the following conditions or medications?

Accepted Answer

Quinidine

Answer

Hyperkalemia

Answer

Hypomagnesemia

Answer

Chronic phenytoin therapy

Question 9

Which of the following muscle relaxants is contraindicated in muscular dystrophy?

Accepted Answer

Succinylcholine

Answer

Quinine

Answer

Dantrolene

Answer

All of the above

Question 10

A 35-year-old patient is given excessive intravenous Benzodiazepine. She suddenly becomes agitated, combative, and exhibits involuntary movements. The anesthesiologist determines that she is having a reaction to the drug which has been given in excess. What is the next step in management?

Accepted Answer

Flumazenil

Answer

Protamine

Answer

Buprenorphine

Answer

Morphine

General Anesthesia — MCQs

General Anesthesia — MCQs

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