Adverse Drug Reactions — MCQs
What is the primary clinical use of Sugammadex in anesthesia?
A patient is admitted with insomnia, agitation, diarrhea, dilated pupils, and sweating. What is the type of poisoning?
A child during anesthesia with halothane and succinylcholine develops severe stiffness of masseters. What is the most probable diagnosis?
Diazepam poisoning is treated by:
Malignant hyperthermia is a rare complication of the use of the following anaesthetic:
Which of the following is classified as a Type E adverse reaction?
Treatment of malignant hyperthermia is
An 18 years old woman in the active stage of labour requests an epidural anaesthesia for delivery. Immediately following the epidural injection of 12ml of 2% lidocaine, the patient complains of lip numbness and becomes apprehensive. What is the presumptive diagnosis?
A cardiovascular parameter helpful in diagnosis of anaphylaxis during anaesthesia:
What causes sudden decreased end tidal CO2 in GA?
Adverse Drug Reactions Indian Medical PG Practice Questions and MCQs
Question 1: What is the primary clinical use of Sugammadex in anesthesia?
- A. Organophosphate poisoning
- B. Reversal of NM blockers (Correct Answer)
- C. Treatment of local anaesthetic poisoning
- D. Treatment of central anticholinergic syndrome
Explanation: ***Reversal of NM blockers*** - **Sugammadex** is a modified gamma-cyclodextrin that specifically encapsulates steroidal **neuromuscular blocking agents (NMBAs)** like **rocuronium** and **vecuronium**. - This encapsulation rapidly inactivates the NMBAs, leading to a dose-dependent and swift **reversal of neuromuscular blockade**. *Organophosphate poisoning* - Organophosphate poisoning is treated with **atropine** to block muscarinic effects and **pralidoxime** to reactivate inhibited acetylcholinesterase. - Sugammadex has no role in antagonizing the effects of **organophosphates** or regenerating acetylcholinesterase. *Treatment of local anaesthetic poisoning* - Local anesthetic systemic toxicity (LAST) is primarily managed with supportive care, including airway management, and the administration of **lipid emulsion therapy**. - Sugammadex does not bind to local anesthetics and therefore has no efficacy in treating local anesthetic poisoning. *Treatment of central anticholinergic syndrome* - Central anticholinergic syndrome is typically treated with **physostigmine**, an acetylcholinesterase inhibitor that can cross the blood-brain barrier. - Sugammadex is not an anticholinergic antagonist and does not affect the central nervous system to reverse anticholinergic effects.
Question 2: A patient is admitted with insomnia, agitation, diarrhea, dilated pupils, and sweating. What is the type of poisoning?
- A. Cannabis
- B. Ecstasy
- C. Heroin
- D. Cocaine (Correct Answer)
Explanation: **Cocaine** - The symptoms of **insomnia, agitation, diarrhea, dilated pupils, and sweating** are classic manifestations of **sympathomimetic toxicity**, characteristic of cocaine poisoning. - Cocaine acts by **blocking the reuptake of norepinephrine, dopamine, and serotonin**, leading to excessive stimulation of the central and peripheral nervous systems. - This presentation represents a **pure sympathomimetic toxidrome** without additional complicating features, which is most classically associated with cocaine intoxication. *Heroin* - Heroin poisoning (opioid overdose) typically presents with **CNS depression**, including **respiratory depression**, **pinpoint pupils (miosis)**, and **constipation**, which are opposite to the symptoms described. - Patients are usually **sedated or comatose**, not agitated or insomniac. - This represents an **opioid toxidrome**, not a sympathomimetic one. *Cannabis* - Cannabis intoxication usually causes **conjunctival injection (red eyes)**, **tachycardia**, **dry mouth**, and **increased appetite**, often accompanied by euphoria or drowsiness. - While it can cause some anxiety/agitation in higher doses or naive users, it does **not cause mydriasis (dilated pupils)** or the severe physical stimulation seen here. - Cannabis does not produce a sympathomimetic toxidrome. *Ecstasy* - Ecstasy (MDMA) is also a sympathomimetic and can cause similar symptoms including agitation, dilated pupils, and sweating. - However, MDMA intoxication is more characteristically associated with **severe hyperthermia**, **hyponatremia**, **bruxism (teeth grinding)**, **serotonin syndrome**, and **rhabdomyolysis** in severe cases. - While both are sympathomimetics, the presentation described represents a **classic pure sympathomimetic picture** most consistent with **cocaine**, which is the more common cause of this toxidrome in clinical practice.
Question 3: A child during anesthesia with halothane and succinylcholine develops severe stiffness of masseters. What is the most probable diagnosis?
- A. Malignant hyperthermia (Correct Answer)
- B. Halothane hepatitis
- C. Neuroleptic malignant syndrome
- D. Anaphylaxis
Explanation: ***Malignant hyperthermia*** - **Masseter muscle rigidity** following exposure to **succinylcholine** and a **halogenated inhalational anesthetic** (like halothane) is a hallmark sign of malignant hyperthermia. - This inherited disorder results in uncontrolled **calcium release** from the sarcoplasmic reticulum in skeletal muscle, leading to hypermetabolism, severe muscle contraction, and a rapid rise in body temperature. *Halothane hepatitis* - This is an idiosyncratic liver injury that can occur hours to days after exposure to halothane, not an acute intraoperative event causing muscle stiffness. - Symptoms include elevated liver enzymes, jaundice, and often fever, but without the immediate muscle rigidity seen here. *Neuroleptic malignant syndrome* - This condition is associated with the use of **antipsychotic medications** and presents with muscle rigidity, fever, altered mental status, and autonomic instability. - It does not involve exposure to succinylcholine or inhalational anesthetics and has a slower onset, typically over days. *Anaphylaxis* - Anaphylaxis is a severe, acute allergic reaction characterized by **bronchospasm**, **hypotension**, **urticaria**, and angioedema. - While it can manifest rapidly during anesthesia, it does not typically cause severe, generalized muscle stiffness as the primary symptom.
Question 4: Diazepam poisoning is treated by:
- A. Resins
- B. Hemofiltration
- C. Charcoal
- D. Flumazenil (Correct Answer)
Explanation: ***Flumazenil*** - **Flumazenil** is a **benzodiazepine receptor antagonist** that competitively binds to the benzodiazepine binding site on the GABA-A receptor, reversing the effects of diazepam. - It is used in cases of severe benzodiazepine overdose causing **respiratory depression** or **severe sedation**. *Resins* - **Resins**, such as **cholestyramine**, are typically used to bind toxins or drugs in the **gastrointestinal tract** that undergo enterohepatic recirculation. - They are generally not effective for reversing the central nervous system depression caused by a benzodiazepine overdose. *Hemofiltration* - **Hemofiltration** is a form of renal replacement therapy used to remove small and middle molecular weight substances from the blood. - While it can remove some drugs, **diazepam** is highly **lipophilic** and extensively **protein-bound**, making it poorly amenable to removal by hemofiltration. *Charcoal* - **Activated charcoal** is used to prevent the absorption of ingested toxins from the gastrointestinal tract. - It is effective when administered soon after ingestion but does not reverse the established effects of an absorbed drug like diazepam in an overdose situation.
Question 5: Malignant hyperthermia is a rare complication of the use of the following anaesthetic:
- A. Thiopentone sodium
- B. Halothane (Correct Answer)
- C. Ether
- D. Ketamine
Explanation: **Halothane** - **Halothane** is a potent volatile anesthetic and a classic trigger for **malignant hyperthermia** due to its effect on ryanodine receptors, leading to excessive calcium release from the sarcoplasmic reticulum. - While its use has declined, it remains a critical example of an anesthetic agent known to induce this life-threatening genetic disorder. *Thiopentone Sodium* - **Thiopentone sodium** is an intravenous barbiturate anesthetic and is **not associated** with triggering malignant hyperthermia. - It is often used for induction of anesthesia and has a different mechanism of action involving GABA receptors. *Ether* - **Diethyl ether** was one of the earliest general anesthetics but is **not a trigger** for malignant hyperthermia. - Its use has largely been discontinued due to its flammability and adverse side effects, but it doesn't cause MH. *Ketamine* - **Ketamine** is a dissociative anesthetic that acts as an NMDA receptor antagonist and is **not a trigger** for malignant hyperthermia. - It is often used for its analgesic and sedative properties and is considered safe in patients susceptible to MH.
Question 6: Which of the following is classified as a Type E adverse reaction?
- A. Toxicity
- B. Augmented effect
- C. Teratogenesis
- D. Rebound effect due to drug withdrawal (Correct Answer)
Explanation: ***Rebound effect due to drug withdrawal*** - Type E adverse reactions are related to **end-of-treatment effects**, specifically withdrawal phenomena. - The **rebound effect** after drug cessation, such as worsened angina after stopping beta-blockers, is a classic example of a Type E reaction. *Toxicity* - This is a general term for adverse effects from excessive drug doses and is **not a specific type** in the ABCDEF classification. - Dose-dependent toxic effects typically align with **Type A** (augmented) reactions, which are predictable and related to the drug's pharmacology. *Augmented effect* - An **augmented effect** is classified as a Type A adverse drug reaction, meaning it is **dose-dependent**, predictable from the drug's known pharmacology, and common. - Examples include bleeding with anticoagulants or hypotension with antihypertensives. *Teratogenesis* - **Teratogenesis** refers to drug-induced fetal malformations and is categorized as a **Type D** (delayed) adverse drug reaction. - These effects are often severe, occur after prolonged exposure, and are rare.
Question 7: Treatment of malignant hyperthermia is
- A. Propranolol
- B. Dantrolene (Correct Answer)
- C. Halothane
- D. Nitrous oxide
Explanation: ***Dantrolene*** - **Dantrolene** is a **ryanodine receptor antagonist** that blocks calcium release from the sarcoplasmic reticulum in muscle cells, directly addressing the underlying pathophysiology of malignant hyperthermia. - Administration of dantrolene is the **first-line and specific treatment** for malignant hyperthermia, rapidly reversing its life-threatening symptoms. *Propranolol* - **Propranolol** is a **beta-blocker** primarily used to treat hypertension, angina, and arrhythmias, by reducing heart rate and contractility. - It does not have any direct action on the **ryanodine receptors** or the excessive calcium release responsible for the muscle rigidity and hypermetabolism seen in malignant hyperthermia. *Halothane* - **Halothane** is an **inhalational anesthetic** that is a well-known trigger of malignant hyperthermia, particularly in genetically susceptible individuals. - Administering halothane would **exacerbate** malignant hyperthermia due to its potent ability to induce uncontrolled calcium release from the sarcoplasmic reticulum. *Nitrous oxide* - **Nitrous oxide** is an **inhalational anesthetic** that is generally considered a weak trigger for malignant hyperthermia and is often used in combination with other agents. - While typically considered safe regarding malignant hyperthermia, it does not possess any therapeutic properties to treat the condition and would not be used once malignant hyperthermia is suspected.
Question 8: An 18 years old woman in the active stage of labour requests an epidural anaesthesia for delivery. Immediately following the epidural injection of 12ml of 2% lidocaine, the patient complains of lip numbness and becomes apprehensive. What is the presumptive diagnosis?
- A. Allergy to drug administered
- B. Systemic toxicity to drug administered (Correct Answer)
- C. Vasovagal shock
- D. Drug entered SA space
Explanation: ***Systemic toxicity to drug administered*** - **Lip numbness** and apprehension immediately following epidural lidocaine injection are classic signs of **local anesthetic systemic toxicity (LAST)** due to unintended intravascular injection. - The rapid onset of symptoms suggests direct access to the systemic circulation via a blood vessel, leading to high plasma concentrations of lidocaine. *Allergy to drug administered* - Allergic reactions to local anesthetics are rare and typically involve **urticaria**, **bronchospasm**, or **anaphylaxis**, which are not described here. - Symptoms of allergy usually do not include lip numbness and apprehension as the primary manifestations. *Vasovagal shock* - Vasovagal reactions are characterized by **bradycardia**, **hypotension**, and syncope, usually triggered by pain or anxiety. - While apprehension is present, the specific symptom of lip numbness is not typical of a vasovagal response. *Drug entered SA space* - If the drug had entered the subarachnoid (SA) space, the patient would likely experience a **rapid onset of profound motor and sensory block**, potentially leading to **total spinal anesthesia** and respiratory compromise. - Lip numbness and apprehension are not primary indicators of inadvertent subarachnoid injection; rather, they point to systemic absorption.
Question 9: A cardiovascular parameter helpful in diagnosis of anaphylaxis during anaesthesia:
- A. Bradycardia
- B. Dysrhythmia
- C. Increased peripheral vascular resistance
- D. Hypotension (Correct Answer)
Explanation: ***Hypotension*** - **Hypotension** is a hallmark cardiovascular sign of anaphylaxis, occurring due to widespread **vasodilation** and increased vascular permeability. - This symptom is often profound and unresponsive to initial fluid resuscitation due to the ongoing systemic release of inflammatory mediators. *Bradycardia* - While bradycardia can occur in some rare cases of anaphylaxis (e.g., **vasovagal response**), **tachycardia** is the more common cardiac response due to compensatory mechanisms. - It is not a primary or consistent indicator of anaphylaxis, making it less helpful for diagnosis in this context. *Dysrhythmia* - **Dysrhythmias** can occur during anaphylaxis due to myocardial ischemia or electrolyte imbalances, but they are not a direct or consistent diagnostic feature. - Their presence often reflects severe compromise or co-existing conditions rather than being a primary anaphylactic sign. *Increased peripheral vascular resistance* - Anaphylaxis is characterized by a significant **decrease in peripheral vascular resistance** due to mast cell and basophil degranulation releasing vasodilatory mediators like histamine. - Therefore, an increase in peripheral vascular resistance would contradict the pathophysiology of anaphylaxis.
Question 10: What causes sudden decreased end tidal CO2 in GA?
- A. Cardiac arrest (Correct Answer)
- B. Pulmonary embolism
- C. Pulmonary hypertension
- D. Malignant hyperthermia
Explanation: ***Cardiac arrest*** - In **cardiac arrest**, there is a sudden cessation of effective **cardiac output**, which leads to a dramatic reduction in pulmonary blood flow. - As a result, **CO2 is not transported to the lungs** for exhalation, causing an abrupt and severe drop in **end-tidal CO2**. *Pulmonary embolism* - A **pulmonary embolism** causes an acute obstruction of pulmonary arterial blood flow, leading to an **increase in alveolar dead space**. - While it can decrease **end-tidal CO2** due to reduced perfusion, the drop is often less sudden and complete than in cardiac arrest, and the primary mechanism is **ventilation-perfusion mismatch**. *Pulmonary hypertension* - **Pulmonary hypertension** involves chronically elevated pressures in the pulmonary arteries, which can lead to **right ventricular dysfunction** and reduced cardiac output over time. - It typically causes a more gradual and chronic reduction in **end-tidal CO2** due to impaired gas exchange, rather than a sudden, precipitous drop. *Malignant hyperthermia* - **Malignant hyperthermia** is characterized by a rapid and severe increase in **metabolic rate** and CO2 production. - This condition typically leads to a **sudden increase in end-tidal CO2** as the body produces more CO2 than can be eliminated, rather than a decrease.
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