Adjuvant Analgesics — MCQs
Which of the following is the most appropriate pharmacological treatment for neuropathic pain in a diabetic patient?
Which of the following actions is NOT associated with tricyclic antidepressants?
Which is a GABA transaminase inhibitor?
Which of the following anaesthetic agent lacks analgesic effect? A) N2O B) Thiopentone C) Methohexitone D) Ketamine E) Fentanyl
Clonidine is used as an antihypertensive agent, but if used as a fast intravenous injection, it can increase blood pressure due to:
Match the following drugs in Column A with their contraindications in Column B. | Column A | Column B | | :-- | :-- | | 1. Morphine | 1. QT prolongation | | 2. Amiodarone | 2. Thromboembolism | | 3. Vigabatrin | 3. Pregnancy | | 4. Estrogen preparations | 4. Head injury |
The cardiovascular side effects of Dexmedetomidine are as follows:
After chronic use of steroids, a patient presents with severe pain in the right hip and immobility. What is the most likely diagnosis?
Which intravenous anaesthetic agent has analgesic effect also
Which of the following agents is used for the treatment of post operative shivering?
Adjuvant Analgesics Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following is the most appropriate pharmacological treatment for neuropathic pain in a diabetic patient?
- A. Acetaminophen
- B. Tramadol
- C. Aspirin
- D. Gabapentin (Correct Answer)
Explanation: ***Gabapentin*** - **Gabapentin** is a widely recommended first-line treatment for diabetic neuropathic pain due to its efficacy in modulating neuronal excitability. - It works by binding to the **α2δ subunit of voltage-gated calcium channels**, reducing calcium influx and thereby decreasing the release of excitatory neurotransmitters involved in pain signaling. *Acetaminophen* - **Acetaminophen** is primarily an analgesic and antipyretic, effective for mild to moderate non-neuropathic pain. - It has no significant efficacy against **neuropathic pain**, which involves distinct neurobiological mechanisms. *Tramadol* - **Tramadol** is an opioid analgesic with some serotonin and norepinephrine reuptake inhibition, offering moderate pain relief. - While it can be used for moderate to severe pain, it is generally considered a **second-line agent** for neuropathic pain due to its opioid nature and potential side effects. *Aspirin* - **Aspirin** is a nonsteroidal anti-inflammatory drug (NSAID) primarily used for its anti-inflammatory, analgesic, and antiplatelet effects. - It is **ineffective for neuropathic pain**, which does not typically involve peripheral inflammation as its primary mechanism.
Question 2: Which of the following actions is NOT associated with tricyclic antidepressants?
- A. Block 5-HT or NE reuptake
- B. Anticholinergic action
- C. MAO inhibition (Correct Answer)
- D. Causes sedation
Explanation: ***MAO inhibition*** - Tricyclic antidepressants (TCAs) primarily exert their effects by inhibiting the reuptake of **norepinephrine** and **serotonin**, not by inhibiting monoamine oxidase (MAO). - **MAO inhibitors** are a distinct class of antidepressants with a different mechanism of action and side effect profile. *Anticholinergic action* - Many TCAs have significant **anticholinergic effects**, blocking muscarinic receptors and leading to side effects like dry mouth, constipation, and blurred vision. - These effects contribute to the **adverse event profile** of TCAs, especially in elderly patients. *Block 5-HT or NE reuptake* - The primary mechanism of action of TCAs involves the **inhibition of serotonin (5-HT)** and **norepinephrine (NE) reuptake** into presynaptic neurons. - This action increases the concentration of these neurotransmitters in the **synaptic cleft**, thereby potentiating their effects. *Causes sedation* - TCAs frequently cause **sedation**, particularly the more histaminergic ones (e.g., amitriptyline, doxepin), due to their **histamine H1 receptor antagonism**. - This side effect can be beneficial for patients with insomnia but can be problematic for daytime functioning.
Question 3: Which is a GABA transaminase inhibitor?
- A. TCA
- B. Valproate (Correct Answer)
- C. Gabapentin
- D. Sertraline
Explanation: ***Valproate*** - Valproate is known to inhibit **GABA transaminase**, an enzyme responsible for the breakdown of **gamma-aminobutyric acid (GABA)**. - By inhibiting this enzyme, valproate increases the concentration of **GABA** in the brain, enhancing its inhibitory effects and contributing to its anticonvulsant properties. *TCA* - **Tricyclic antidepressants (TCAs)** primarily work by inhibiting the reuptake of **norepinephrine** and **serotonin** in the brain. - They do not directly inhibit GABA transaminase but rather modulate monoamine neurotransmission. *Sertraline* - **Sertraline** is a **selective serotonin reuptake inhibitor (SSRI)** that works by blocking the reabsorption of **serotonin** into presynaptic neurons. - Its primary mechanism of action is focused on serotonin pathways, not on GABA metabolism. *Gabapentin* - **Gabapentin** is an anticonvulsant that is thought to exert its effects by modulating **calcium channels** and increasing **GABA synthesis**, but it is not a direct inhibitor of GABA transaminase. - Its mechanism of action is distinct from directly preventing GABA breakdown.
Question 4: Which of the following anaesthetic agent lacks analgesic effect? A) N2O B) Thiopentone C) Methohexitone D) Ketamine E) Fentanyl
- A. N2O
- B. Methohexitone
- C. Ketamine
- D. Fentanyl
- E. Thiopentone (Correct Answer)
Explanation: ***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.
Question 5: Clonidine is used as an antihypertensive agent, but if used as a fast intravenous injection, it can increase blood pressure due to:
- A. Agonistic action on vascular Alpha 2 adrenergic receptors (Correct Answer)
- B. Cardiac stimulation
- C. Stimulation of the vasomotor center leading to increased sympathetic output
- D. Release of noradrenaline from adrenergic nerve endings
Explanation: ***Agonistic action on vascular Alpha 2 adrenergic receptors*** - When administered rapidly intravenously, clonidine initially acts as an agonist on **postsynaptic α2-adrenergic receptors** in the vascular smooth muscle. - This direct peripheral vasoconstrictive effect occurs before central effects dominate, leading to a transient increase in blood pressure. *Stimulation of the vasomotor center leading to increased sympathetic output* - Clonidine's primary antihypertensive effect is through **central α2-receptor agonism**, which *decreases* sympathetic outflow from the vasomotor center. - It would not stimulate the vasomotor center to *increase* sympathetic output, as this contradicts its fundamental mechanism of action. *Cardiac stimulation* - Clonidine is known for its **cardiac depressant effects** due to reduced sympathetic outflow, leading to decreased heart rate and contractility. - It does not directly stimulate the heart, and any initial blood pressure rise is due to vascular effects, not increased cardiac output. *Release of noradrenaline from adrenergic nerve endings* - Clonidine is an **α2-adrenergic agonist**, and activation of presynaptic α2-receptors typically *inhibits* the release of noradrenaline. - It does not cause a direct release of noradrenaline but rather modulates its release in the opposite direction.
Question 6: Match the following drugs in Column A with their contraindications in Column B. | Column A | Column B | | :-- | :-- | | 1. Morphine | 1. QT prolongation | | 2. Amiodarone | 2. Thromboembolism | | 3. Vigabatrin | 3. Pregnancy | | 4. Estrogen preparations | 4. Head injury |
- A. A-1, B-3, C-2, D-4
- B. A-4, B-1, C-3, D-2 (Correct Answer)
- C. A-3, B-2, C-4, D-1
- D. A-2, B-4, C-1, D-3
Explanation: ***A-4, B-1, C-3, D-2*** - **Morphine** is contraindicated in **head injury** as it can increase intracranial pressure and mask neurological symptoms. - **Amiodarone** is contraindicated in patients with **QT prolongation** due to its risk of inducing more severe arrhythmias like Torsades de Pointes. - **Vigabatrin** is contraindicated during **pregnancy** due to its potential for teratogenicity and adverse effects on fetal development. - **Estrogen preparations** are contraindicated in patients with a history of **thromboembolism** due to their increased risk of blood clot formation. *A-1, B-3, C-2, D-4* - This option incorrectly matches **Morphine** with QT prolongation and **Estrogen preparations** with head injury, which are not their primary contraindications. - It also incorrectly links **Vigabatrin** with thromboembolism and **Amiodarone** with pregnancy. *A-3, B-2, C-4, D-1* - This choice incorrectly associates **Morphine** with pregnancy and **Vigabatrin** with head injury, which are not the most critical or direct contraindications. - It also misaligns **Amiodarone** with thromboembolism and **Estrogen preparations** with QT prolongation. *A-2, B-4, C-1, D-3* - This option incorrectly matches **Morphine** with thromboembolism and **Amiodarone** with head injury, which are not their most significant contraindications. - It also incorrectly links **Vigabatrin** with QT prolongation and **Estrogen preparations** with pregnancy.
Question 7: The cardiovascular side effects of Dexmedetomidine are as follows:
- A. Hypertension and Tachycardia
- B. Hypertension and Bradycardia
- C. Hypotension and Bradycardia (Correct Answer)
- D. Hypotension and Tachycardia
Explanation: ***Hypotension and Bradycardia*** - **Dexmedetomidine** is an **alpha-2 adrenergic agonist** that causes a dose-dependent decrease in heart rate (bradycardia) and blood pressure (hypotension) due to reduced sympathetic outflow. - The initial hypertensive effect seen with rapid IV administration is usually transient and followed by sustained hypotension. *Hypertension and Tachycardia* - This combination is not typical for **dexmedetomidine**, which primarily exerts its effects by centrally reducing sympathetic tone, leading to lowered heart rate and blood pressure. - **Tachycardia** is a rare and usually reflex-mediated response if severe hypotension occurs, but it's not a primary effect. *Hypertension and Bradycardia* - While an initial, transient **hypertension** can occur with rapid **dexmedetomidine** infusion due to peripheral alpha-2 stimulation, this is not its predominant long-term cardiovascular effect. - The sustained effect is usually **hypotension**, not hypertension, making this option incorrect as a primary side effect. *Hypotension and Tachycardia* - Although **hypotension** is a common side effect of **dexmedetomidine**, **tachycardia** is generally not. - The drug mainly causes a reduction in heart rate (**bradycardia**) as part of its central sympatholytic action.
Question 8: After chronic use of steroids, a patient presents with severe pain in the right hip and immobility. What is the most likely diagnosis?
- A. Avascular necrosis (Correct Answer)
- B. Hip dislocation
- C. Osteoarthritis
- D. Perthes disease
Explanation: ***Avascular necrosis*** - Chronic **steroid use** is a major risk factor for avascular necrosis (AVN), particularly affecting the **femoral head**, leading to severe hip pain and immobility. - AVN occurs due to the death of bone tissue resulting from an **interruption of blood supply**, often manifesting as pain that worsens with weight-bearing. *Perthes disease* - This condition is a form of avascular necrosis of the femoral head, but it primarily affects **children**, typically between 4 and 10 years old. - The patient's age (adult) makes Perthes disease an unlikely diagnosis. *Hip dislocation* - Hip dislocation presents with **acute, severe pain** and an inability to bear weight, often following significant trauma. - There is no mention of trauma, and the patient has a history of chronic steroid use, which is not a direct cause of hip dislocation. *Osteoarthritis* - While osteoarthritis causes hip pain and stiffness, it typically develops **gradually** and is associated with aging, obesity, or previous joint injury. - The acute, severe pain after chronic steroid use is more characteristic of avascular necrosis.
Question 9: Which intravenous anaesthetic agent has analgesic effect also
- A. Thiopentone
- B. Ketamine (Correct Answer)
- C. Propofol
- D. Etomidate
Explanation: ***Ketamine*** - Ketamine acts as an **N-methyl-D-aspartate (NMDA) receptor antagonist**, providing significant **analgesia** in addition to its anaesthetic effects. - It induces a state of **dissociative anaesthesia**, where the patient appears awake but is unresponsive to pain, making it unique among intravenous anaesthetics. *Thiopentone* - Thiopentone is a **barbiturate** that acts as a potent hypnotic and anaesthetic but provides no significant analgesic properties. - It can even cause **anti-analgesia** (hyperalgesia) at sub-hypnotic doses, increasing sensitivity to pain. *Propofol* - Propofol is a potent intravenous anaesthetic that works primarily as a **GABA-A receptor agonist**, but it lacks intrinsic analgesic properties. - While it can cause some sedation and reduced pain perception due to CNS depression, it does not directly modulate pain pathways in the way an analgesic would. *Etomidate* - Etomidate is a hypnotic agent highly valued for its **cardiovascular stability**, making it suitable for patients with compromised cardiac function. - Like propofol and thiopentone, etomidate primarily acts on **GABA-A receptors** to induce unconsciousness and offers no significant analgesic effects.
Question 10: Which of the following agents is used for the treatment of post operative shivering?
- A. Atropine
- B. Thiopentone
- C. Pethidine (Correct Answer)
- D. Suxamethonium
Explanation: ***Pethidine*** - **Pethidine (meperidine)** is a **synthetic opioid** known for its **mu-receptor agonism** and weak anticholinergic properties, making it effective in treating **post-operative shivering**. - Its mechanism in reducing shivering is thought to involve modulation of the **thermoregulatory center** in the hypothalamus. *Atropine* - **Atropine** is an **anticholinergic drug** that primarily blocks muscarinic acetylcholine receptors, leading to effects like increased heart rate and decreased secretions. - It does not directly act on the thermoregulatory centers or muscle activity responsible for shivering. *Thiopentone* - **Thiopentone** is a **barbiturate** used as an intravenous anesthetic, primarily for induction of anesthesia. - While it has CNS depressant effects, it is not indicated or effective for the specific treatment of post-operative shivering. *Suxamethonium* - **Suxamethonium (succinylcholine)** is a **depolarizing neuromuscular blocker** used to induce muscle paralysis, typically for intubation. - It would prevent shivering by paralyzing skeletal muscles, but this is a dangerous and inappropriate treatment for shivering due to its profound respiratory depressant effects.
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