Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs Indian Medical PG Practice Questions and MCQs

Question 161: Which uricosuric drug is not used in acute gout?

A. NSAIDs
B. Colchicine
C. Corticosteroids
D. Sulfinpyrazone (Correct Answer)

Explanation: **Explanation:** The management of gout is divided into two distinct phases: **Acute Gouty Arthritis** (treatment of inflammation) and **Chronic Gout** (lowering serum uric acid levels). **Why Sulfinpyrazone is the correct answer:** Sulfinpyrazone is a **uricosuric agent**. It works by inhibiting the reabsorption of uric acid in the proximal convoluted tubules of the kidney, thereby increasing uric acid excretion. Uricosuric drugs (and Xanthine Oxidase inhibitors like Allopurinol) should **never** be initiated during an acute attack. Rapid fluctuations in serum uric acid levels can cause the mobilization of urate crystals from tissue stores, which paradoxically worsens and prolongs the acute inflammatory episode. **Analysis of Incorrect Options:** * **A. NSAIDs:** These are the first-line treatment for acute gout. They act by inhibiting prostaglandin synthesis, thereby reducing pain and inflammation. (Note: Aspirin is avoided as it can interfere with uric acid excretion). * **B. Colchicine:** This is a classic drug for acute gout. It inhibits microtubule polymerization and leukocyte migration to the joint, effectively halting the inflammatory response. * **C. Corticosteroids:** These are used in acute gout when NSAIDs or Colchicine are contraindicated (e.g., in renal failure) or when the attack is polyarticular. They provide potent anti-inflammatory relief. **NEET-PG High-Yield Pearls:** * **The "Golden Rule":** Never start or stop urate-lowering therapy (ULT) during an acute attack. If a patient is already on ULT when an attack starts, continue it at the same dose. * **Probenecid:** Another uricosuric drug; like Sulfinpyrazone, it is contraindicated in patients with a history of renal stones (urolithiasis). * **Drug of Choice:** NSAIDs (specifically Indomethacin or Naproxen) are generally preferred over Colchicine due to the latter's narrow therapeutic index and GI side effects.

Question 162: Which of the following agents decreases gastric motility?

A. Naloxone (Correct Answer)
B. Morphine
C. Codeine
D. Pethidine

Explanation: **Explanation:** The question focuses on the pharmacological effects of opioids and their antagonists on the gastrointestinal (GI) tract. **1. Why Naloxone is the Correct Answer:** Opioid receptors (primarily **$\mu$-receptors**) are located in the myenteric plexus of the gut. Activation of these receptors inhibits the release of acetylcholine, leading to decreased peristalsis and constipation. **Naloxone** is a competitive opioid receptor antagonist. By blocking these receptors, it reverses opioid-induced inhibition, thereby **increasing** gastric motility and intestinal transit. *Note: There appears to be a discrepancy in the provided key. In standard pharmacology, Morphine, Codeine, and Pethidine **decrease** motility (causing constipation), while Naloxone **increases** it. If the question asks which agent "decreases" motility, the correct options would be B, C, or D. However, if the question asks which agent is used to **reverse** decreased motility or if the key identifies Naloxone as the answer to a "reversal" mechanism, it acts as a prokinetic in the presence of opioids.* **2. Why the Other Options are Incorrect:** * **Morphine:** A prototypical $\mu$-opioid agonist. It significantly **decreases** gastric motility and increases sphincter tone, leading to its notorious side effect: constipation. * **Codeine:** A weaker opioid agonist used for cough and mild pain. Like morphine, it **decreases** GI motility and is often used therapeutically for diarrhea. * **Pethidine (Meperidine):** Though it has some anticholinergic properties, its primary effect as an opioid agonist is to **decrease** gastric emptying and intestinal motility. **3. NEET-PG High-Yield Pearls:** * **Methylnaltrexone & Alvimopan:** These are peripheral $\mu$-opioid antagonists that do not cross the blood-brain barrier. They are specifically used to treat **Opioid-Induced Constipation (OIC)** and postoperative ileus without reversing analgesia. * **Loperamide:** An opioid agonist that does not cross the BBB; used exclusively as an anti-diarrheal because it **decreases** motility. * **Drug of Choice:** Naloxone is the DOC for acute opioid poisoning (given IV).

Question 163: Which of the following drugs reduces the activity of phospholipase A2?

A. Alprostadil
B. Aspirin
C. Ibuprofen
D. Prednisolone (Correct Answer)

Explanation: **Explanation:** The correct answer is **Prednisolone**. **Mechanism of Action:** Prednisolone is a glucocorticoid. Corticosteroids exert their anti-inflammatory effects by inducing the synthesis of **Lipocortin-1 (Annexin A1)**. Lipocortin-1 directly inhibits the enzyme **Phospholipase A2 (PLA2)**. Since PLA2 is responsible for releasing arachidonic acid from membrane phospholipids, its inhibition prevents the formation of all downstream inflammatory mediators, including prostaglandins, thromboxanes, and leukotrienes. **Analysis of Incorrect Options:** * **A. Alprostadil:** This is a synthetic analogue of **Prostaglandin E1 (PGE1)**. It acts as a vasodilator and is used clinically to maintain the patency of the ductus arteriosus or to treat erectile dysfunction. It does not inhibit PLA2. * **B. Aspirin:** This is a Non-Steroidal Anti-Inflammatory Drug (NSAID) that acts further down the cascade. It **irreversibly inhibits Cyclooxygenase (COX-1 and COX-2)** enzymes, preventing the conversion of arachidonic acid into prostaglandins. * **C. Ibuprofen:** Like aspirin, this is an NSAID. It **reversibly inhibits COX-1 and COX-2**. It has no effect on Phospholipase A2. **NEET-PG High-Yield Pearls:** * **Corticosteroids** are the only class that inhibits both the COX and LOX pathways by acting at the level of PLA2. * **Zileuton** inhibits 5-Lipoxygenase (LOX), while **Montelukast/Zafirlukast** are leukotriene receptor antagonists. * **Aspirin** is unique among NSAIDs for its irreversible inhibition (via acetylation) of the COX enzyme, which is why its anti-platelet effect lasts for the life of the platelet (7–10 days).

Question 164: Which of the following is not a vasodilator?

A. Prostacyclin (PGI2)
B. Lipoxin
C. Leukotriene C4 (Correct Answer)
D. Prostaglandin E2 (PGE2)

Explanation: ### Explanation The correct answer is **Leukotriene C4 (LTC4)**. The question tests your knowledge of the vascular effects of various eicosanoids (derivatives of arachidonic acid). **1. Why Leukotriene C4 is the correct answer:** Leukotrienes C4, D4, and E4 (collectively known as cysteinyl leukotrienes) are potent **vasoconstrictors**. They are primarily produced by mast cells and basophils. In addition to vasoconstriction, they cause intense bronchoconstriction and increase vascular permeability (leading to edema), making them key mediators in the pathogenesis of bronchial asthma and anaphylaxis. **2. Why the other options are incorrect:** * **Prostacyclin (PGI2):** Produced by vascular endothelium, it is a potent **vasodilator** and the most powerful endogenous inhibitor of platelet aggregation. * **Lipoxin (LXA4/LXB4):** These are anti-inflammatory mediators. Lipoxin A4 specifically induces **vasodilation** and inhibits neutrophil chemotaxis, acting as a "stop signal" for inflammation. * **Prostaglandin E2 (PGE2):** This is a major mediator of inflammation that causes **vasodilation** (hyperemia) and sensitizes nerve endings to pain (hyperalgesia). **3. NEET-PG High-Yield Clinical Pearls:** * **LTC4, LTD4, LTE4:** Known as the "Slow Reacting Substance of Anaphylaxis" (SRS-A). * **LTB4:** A potent chemotactic agent for neutrophils (Remember: **B**4 for "**B**e there" – attracts cells). * **PGI2 vs. Thromboxane A2 (TXA2):** They have opposing effects. PGI2 (Endothelium) = Vasodilation + Anti-aggregation; TXA2 (Platelets) = Vasoconstriction + Pro-aggregation. * **Aspirin-induced Asthma:** Caused by the shunting of arachidonic acid toward the lipoxygenase pathway (increasing leukotrienes) when the COX pathway is blocked.

Question 165: Which of the following is an IL-1 antagonist?

A. Anakinra (Correct Answer)
B. Abatacept
C. Adalimumab
D. Leflunomide

Explanation: **Explanation:** **Correct Answer: A. Anakinra** Anakinra is a recombinant, non-glycosylated form of the human **Interleukin-1 receptor antagonist (IL-1Ra)**. It works by competitively inhibiting the binding of IL-1α and IL-1β to the Interleukin-1 type I receptor. Since IL-1 is a key mediator of inflammation and joint destruction in Rheumatoid Arthritis (RA), Anakinra helps reduce the inflammatory response. **Analysis of Incorrect Options:** * **B. Abatacept:** This is a **T-cell costimulation modulator**. It consists of the extracellular domain of CTLA-4 fused to a modified Fc portion of human IgG1. It binds to CD80/86 on antigen-presenting cells, preventing the required "second signal" for T-cell activation. * **C. Adalimumab:** This is a fully human monoclonal antibody against **TNF-α** (Tumor Necrosis Factor-alpha). It neutralizes soluble and membrane-bound TNF-α. * **D. Leflunomide:** This is a **DMARD** (Disease-Modifying Antirheumatic Drug) that acts as a prodrug. Its active metabolite (teriflunomide) inhibits the enzyme **dihydroorotate dehydrogenase**, leading to decreased pyrimidine synthesis and inhibition of T-cell proliferation. **High-Yield NEET-PG Pearls:** * **IL-1 Inhibitors:** Apart from Anakinra, other IL-1 inhibitors include **Canakinumab** (monoclonal antibody) and **Rilonacept** (decoy receptor/trap). * **Clinical Use:** Anakinra is used in RA, Neonatal-Onset Multisystem Inflammatory Disease (NOMID), and Gout (off-label for refractory cases). * **Side Effect:** The most common side effect is injection site reactions; it should not be combined with TNF inhibitors due to the high risk of serious infections. * **Leflunomide Fact:** It undergoes extensive enterohepatic circulation; **Cholestyramine** can be used to enhance its clearance in cases of toxicity or pregnancy planning.

Question 166: Tramadol is:

A. Antiflatulent
B. Antireflux drug
C. Beta–blocker
D. Opioid analgesic (Correct Answer)

Explanation: **Explanation:** **Tramadol** is a centrally acting synthetic analogue of codeine used to manage moderate to moderately severe pain. It is classified as an **atypical opioid analgesic** because it possesses a dual mechanism of action: 1. **Mu-opioid receptor agonism:** It (and its active metabolite M1) binds to $\mu$-receptors, though with much lower affinity than morphine. 2. **Monoamine reuptake inhibition:** It inhibits the reuptake of **Norepinephrine and Serotonin (5-HT)** in the spinal cord, enhancing the descending inhibitory pain pathways. **Analysis of Incorrect Options:** * **A & B (Antiflatulent/Antireflux):** These drugs (e.g., Simethicone or PPIs) act on the gastrointestinal tract. While opioids often cause constipation as a side effect, Tramadol has no therapeutic role in treating flatulence or acid reflux. * **C (Beta-blocker):** These agents (e.g., Propranolol) antagonize adrenergic receptors to treat hypertension and arrhythmias. Tramadol does not interact with beta-receptors. **High-Yield Clinical Pearls for NEET-PG:** * **Seizure Risk:** Tramadol lowers the seizure threshold; it is contraindicated in patients with epilepsy or those taking drugs that lower the threshold (e.g., Bupropion, TCAs). * **Serotonin Syndrome:** Due to its effect on 5-HT reuptake, there is a risk of Serotonin Syndrome when co-administered with SSRIs or MAO inhibitors. * **Advantages:** It causes less respiratory depression and has a lower abuse potential compared to traditional opioids like Morphine. * **Antidote:** Respiratory depression caused by Tramadol is only **partially reversed** by Naloxone because of its non-opioid (monoaminergic) component.

Question 167: Which of the following statements about baricitinib is FALSE?

A. Oral JAK inhibitor
B. Approved for use in moderate to severe Crohn's disease (Correct Answer)
C. Increases triglycerides
D. Dose reduction is required in renal and hepatic impairment

Explanation: **Explanation:** **Baricitinib** is a selective and reversible inhibitor of **Janus Kinase (JAK) 1 and 2**. It modulates the signaling pathway of various cytokines (like IL-6, IFN-γ) involved in inflammatory processes. **Why Option B is False (Correct Answer):** While several JAK inhibitors are used in Inflammatory Bowel Disease (IBD), Baricitinib is **not** currently approved for Crohn’s disease. **Upadacitinib** and **Tofacitinib** are the JAK inhibitors typically used in IBD (specifically Ulcerative Colitis). Baricitinib is primarily indicated for **Rheumatoid Arthritis (RA)**, **Alopecia Areata**, and severe **COVID-19**. **Analysis of Other Options:** * **Option A (True):** Baricitinib is an **oral** small-molecule drug, offering an advantage over injectable biological DMARDs. * **Option C (True):** JAK inhibitors are known to cause metabolic alterations, including **hyperlipidemia** (increased LDL, HDL, and triglycerides). Monitoring lipid profiles is mandatory during treatment. * **Option D (True):** Baricitinib is primarily excreted by the kidneys. Dose reduction is required if GFR is between 30-60 mL/min, and it is contraindicated if GFR <30 mL/min. It should also be used with caution in hepatic impairment. **High-Yield NEET-PG Pearls:** 1. **Mechanism:** JAK-STAT pathway inhibition. 2. **Black Box Warning:** Increased risk of serious infections (TB, fungal), malignancies, and **thromboembolism** (DVT/PE). 3. **Specific Indication:** It is the first FDA-approved systemic treatment for **Alopecia Areata**. 4. **Drug Interaction:** Its serum concentration increases when co-administered with **Probenecid** (due to inhibition of OAT3 transporter).

Question 168: What is the mechanism of action of methadone?

A. Opioid receptor agonist (Correct Answer)
B. Opioid receptor partial agonist
C. Opioid receptor antagonist
D. Opioid receptor inverse agonist

Explanation: **Explanation:** **1. Why Option A is Correct:** Methadone is a synthetic, long-acting **μ (mu) opioid receptor agonist**. Its primary mechanism involves binding to and activating mu receptors in the central nervous system, mimicking the effects of endogenous opioids to produce analgesia. Additionally, methadone acts as an **NMDA receptor antagonist** and inhibits the reuptake of serotonin and norepinephrine, which contributes to its efficacy in treating neuropathic pain. **2. Why Other Options are Incorrect:** * **Option B (Partial Agonist):** Buprenorphine is the classic example of a partial mu-agonist. Unlike methadone, partial agonists have a "ceiling effect" on respiratory depression and analgesia. * **Option C (Antagonist):** Naloxone and Naltrexone are opioid antagonists. They bind to receptors with high affinity but produce no biological response, used primarily to reverse opioid overdose. * **Option D (Inverse Agonist):** Naloxone is sometimes characterized as having inverse agonist properties at certain opioid receptors, but methadone strictly activates the receptor, making it an agonist. **3. NEET-PG High-Yield Clinical Pearls:** * **Pharmacokinetics:** Methadone has an exceptionally **long and variable half-life** (15–60 hours), which allows for once-daily dosing in addiction programs but increases the risk of cumulative toxicity. * **Clinical Uses:** It is the gold standard for **Opioid Substitution Therapy (OST)** to manage withdrawal and maintenance in heroin addicts. It is also used for chronic pain management. * **Adverse Effect:** A critical "must-know" side effect for exams is **QT interval prolongation**, which can lead to Torsades de Pointes. * **Metabolism:** It is primarily metabolized by **CYP3A4**; therefore, inhibitors of this enzyme (like ketoconazole) can lead to methadone toxicity.

Question 169: Long term use of pethidine is avoided because a metabolite of pethidine is associated with which of the following?

A. Constipation
B. Dependence
C. Seizures (Correct Answer)
D. Respiratory depression

Explanation: **Explanation:** Pethidine (Meperidine) is a synthetic opioid analgesic. Unlike most opioids, it is not recommended for long-term or chronic pain management due to its metabolic profile. **1. Why Seizures is the Correct Answer:** Pethidine is metabolized in the liver via N-demethylation to its active metabolite, **Norpethidine**. Norpethidine has a longer half-life (15–20 hours) than pethidine (3 hours) and possesses significant **CNS stimulant** properties. With repeated dosing or in patients with renal impairment, norpethidine accumulates, leading to CNS toxicity characterized by tremors, muscle twitches, hyperreflexia, and ultimately, **grand mal seizures**. **2. Analysis of Incorrect Options:** * **A. Constipation:** While pethidine causes less constipation than morphine (due to its mild anticholinergic activity), it is not the reason its *long-term* use is specifically contraindicated. * **B. Dependence:** All mu-opioid agonists carry a risk of dependence; however, this is a class effect and not specifically linked to a toxic metabolite. * **C. Respiratory depression:** This is a common acute side effect of all opioids. While norpethidine can contribute to toxicity, the specific limiting factor for long-term use is the excitatory neurotoxicity (seizures), not respiratory depression. **High-Yield Clinical Pearls for NEET-PG:** * **Anticholinergic effects:** Pethidine is the only opioid that causes **mydriasis** (due to its atropine-like structure) instead of the classic "pinpoint pupil" (miosis). * **Tachycardia:** Unlike other opioids that cause bradycardia, pethidine can cause tachycardia. * **Drug Interaction:** Pethidine is strictly contraindicated with **MAO inhibitors**, as it can precipitate a life-threatening **Serotonin Syndrome** (hyperpyrexia, coma, and convulsions). * **Renal Caution:** Always avoid pethidine in patients with renal failure due to rapid norpethidine accumulation.

Question 170: Which of the following is NOT a first-line drug for treating neuropathic pain?

A. Lidocaine
B. Gabapentin
C. Duloxetine
D. Opioids (Correct Answer)

Explanation: **Explanation:** Neuropathic pain results from damage or dysfunction of the somatosensory nervous system [2]. Unlike nociceptive pain, it responds poorly to conventional analgesics like NSAIDs and is managed using drugs that modulate neurotransmission. **Why Opioids are the Correct Answer:** According to international guidelines (IASP/NeuPSIG), **Opioids** (e.g., Morphine, Oxycodone) are considered **second-line or third-line treatments**. While effective, they are not first-line due to significant risks of dependence, tolerance, opioid-induced hyperalgesia [3], and the potential for misuse. They are generally reserved for patients who fail to respond to first-line agents or for acute exacerbations of severe neuropathic pain. **Analysis of Incorrect Options (First-line Agents):** * **Gabapentin (and Pregabalin):** These are Calcium channel $\alpha_2\delta$ ligands. They reduce the release of excitatory neurotransmitters (Glutamate, Substance P) and are first-line for Post-herpetic neuralgia and Diabetic neuropathy [1]. * **Duloxetine (and Venlafaxine):** These are SNRIs (Serotonin-Norepinephrine Reuptake Inhibitors). They enhance the descending inhibitory pain pathways and are first-line, especially for painful diabetic neuropathy [1]. * **Lidocaine (Topical):** Topical 5% lidocaine patches are considered first-line for **localized** neuropathic pain, such as Post-herpetic neuralgia (PHN), due to their excellent safety profile and minimal systemic absorption. **NEET-PG High-Yield Pearls:** * **Tricyclic Antidepressants (TCAs):** Amitriptyline is also a first-line agent [2] but should be used cautiously in the elderly due to anticholinergic side effects. * **Trigeminal Neuralgia:** The drug of choice is **Carbamazepine** (not Gabapentin). * **Mechanism of Gabapentin:** It does *not* act on GABA receptors; it binds to the $\alpha_2\delta$ subunit of voltage-gated calcium channels.

Practice by Chapter

NSAIDs: Classification and Mechanism

Practice Questions

COX-2 Selective Inhibitors

Practice Questions

Acetaminophen (Paracetamol)

Practice Questions

Opioid Analgesics and Antagonists

Practice Questions

Drugs Used in Gout and Hyperuricemia

Practice Questions

Drugs Used in Rheumatoid Arthritis

Practice Questions

Disease-Modifying Antirheumatic Drugs

Practice Questions

Glucocorticoids as Anti-inflammatory Agents

Practice Questions

Migraine Therapeutics

Practice Questions

Neuropathic Pain Management

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free