Analgesics and Anti-inflammatory Drugs Practice Questions

Q: Which NSAID is proposed to act by inhibition of COX-3?

Paracetamol. **Explanation:** **Correct Answer: B. Paracetamol** Paracetamol (Acetaminophen) is unique among common analgesics because it possesses potent analgesic and antipyretic properties but lacks significant peripheral anti-inflammatory activity. This clinical profile is attributed to its mechanism of action: it primarily inhibits prostaglandin synthesis in the **Central Nervous System (CNS)**. It is proposed that Paracetamol acts by inhibiting **COX-3**, a splice variant of the COX-1 enzyme found predominantly in the cerebral cortex and heart. By inhibiting COX-3, Paracetamol reduces pain and fever without affecting peripheral COX-1 or COX-2, which explains why it does not cause gastric ulcers or anti-platelet effects. **Analysis of Incorrect Options:** * **A. Nimesulide:** A **preferential COX-2 inhibitor**. It is known for its rapid onset of action but is associated with a risk of hepatotoxicity. * **C. Ketorolac:** A **non-selective COX inhibitor** with exceptionally potent analgesic activity. It is primarily used for short-term management of severe acute pain (e.g., post-operative) but has a high risk of GI side effects. * **D. Rofecoxib:** A **selective COX-2 inhibitor**. Most drugs in this class (Coxibs) were withdrawn or restricted due to an increased risk of cardiovascular events (thrombotic strokes and MI). **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Paracetamol is the DOC for fever in children (to avoid Reye’s syndrome associated with Aspirin) and during pregnancy. * **Antidote:** In Paracetamol toxicity (NAPQI accumulation), the antidote is **N-acetylcysteine (NAC)**, which replenishes glutathione stores. * **Key Limitation:** Paracetamol is **not** an NSAID in the functional sense because it lacks anti-inflammatory activity at therapeutic doses.

Q: Which among the following drugs is contraindicated in renal failure?

Pethidine. ### Explanation **Correct Option: A. Pethidine** Pethidine (Meperidine) is strictly contraindicated in renal failure due to its metabolism. It is metabolized in the liver to **Norpethidine**, an active metabolite. Norpethidine has a long half-life and is primarily excreted by the kidneys. In renal impairment, norpethidine accumulates, leading to **CNS toxicity**. This manifests as irritability, tremors, hallucinations, and most characteristically, **seizures**. Unlike pethidine, norpethidine-induced seizures are not reversed by Naloxone; in fact, Naloxone may worsen them by lowering the seizure threshold. **Analysis of Incorrect Options:** * **B. Morphine:** While Morphine should be used with extreme caution in renal failure (due to the accumulation of *Morphine-6-glucuronide*, which causes prolonged respiratory depression), it is generally considered a "relative contraindication" compared to the absolute risk of seizures with Pethidine. * **C. Fentanyl:** This is the **opioid of choice** in renal failure. It has no active metabolites and is primarily cleared by hepatic metabolism, making it safe for patients with impaired kidney function. * **D. Atracurium:** This is a neuromuscular blocker, not an analgesic. It is the **muscle relaxant of choice** in renal failure because it undergoes **Hofmann elimination** (spontaneous non-enzymatic degradation), which is independent of renal or hepatic function. **High-Yield Clinical Pearls for NEET-PG:** * **Pethidine & MAO Inhibitors:** Co-administration can lead to a life-threatening **Serotonin Syndrome** (hyperpyrexia, excitation). * **Pethidine in Obstetrics:** It is often preferred during labor as it causes less inhibition of uterine contractions compared to morphine. * **Drug of Choice for Biliary Colic:** Pethidine is traditionally preferred over morphine because it causes less spasm of the **Sphincter of Oddi**.

Q: Aspirin is associated with which of the following conditions?

Reye's Syndrome. **Explanation:** **Reye’s Syndrome (Correct Answer):** Reye’s Syndrome is a rare but life-threatening condition characterized by **acute encephalopathy** and **fatty degeneration of the liver (microvesicular steatosis)**. It is strongly associated with the use of **Aspirin (salicylates)** in children and adolescents during a viral prodrome, most commonly **Influenza B** or **Varicella**. The underlying pathophysiology involves **mitochondrial dysfunction**, leading to impaired fatty acid oxidation and hyperammonemia. Due to this risk, Aspirin is contraindicated in children under 16 years of age, except in specific conditions like Kawasaki disease. **Incorrect Options:** * **Sjogren Syndrome:** An autoimmune systemic connective tissue disorder characterized by lymphocytic infiltration of exocrine glands, leading to dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia). It has no association with Aspirin. * **Reiter Syndrome (Reactive Arthritis):** A triad of urethritis, conjunctivitis, and arthritis that typically follows a gastrointestinal or genitourinary infection (e.g., Chlamydia). It is an HLA-B27 associated spondyloarthropathy and is not triggered by salicylate use. **High-Yield Clinical Pearls for NEET-PG:** * **Liver Biopsy Finding:** Microvesicular steatosis (no inflammation). * **Biochemical Markers:** Elevated serum ammonia, prolonged Prothrombin Time (PT), and elevated AST/ALT with **normal bilirubin**. * **Management:** Supportive care; IV Mannitol or hypertonic saline may be used to manage cerebral edema. * **Exception:** Aspirin is the drug of choice in **Kawasaki Disease**, despite the theoretical risk of Reye’s Syndrome; in such cases, the Influenza vaccine is strictly recommended.

Q: Acute gouty arthritis is seen early following treatment with which of the following medications?

Allopurinol. **Explanation:** **Why Allopurinol is the Correct Answer:** Allopurinol is a **Xanthine Oxidase Inhibitor** used for the long-term management of chronic gout. When initiated, it causes a rapid decline in serum uric acid levels. This sudden drop triggers the **mobilization and dissolution of urate crystals** (monosodium urate) from tissue stores (tophi) into the joint space. These "naked" crystals are highly pro-inflammatory, leading to the precipitation of an **acute gouty flare**. This phenomenon is known as "mobilization gout." To prevent this, Allopurinol should always be co-administered with low-dose Colchicine or NSAIDs for the first 3–6 months. **Analysis of Incorrect Options:** * **Rasburicase (A):** This is a recombinant urate oxidase enzyme that converts uric acid into allantoin (a highly soluble metabolite). It is primarily used for **Tumor Lysis Syndrome**. While it lowers uric acid rapidly, it is not typically associated with the clinical "flare" seen during chronic gout management. * **Probenecid (B) & Sulfinpyrazone (D):** These are **Uricosuric agents** that inhibit the reabsorption of uric acid in the proximal tubule. While they can theoretically cause flares, Allopurinol is the classic and most common culprit tested in exams regarding treatment-induced acute gouty arthritis. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of Thumb:** Never start Allopurinol during an acute attack of gout; wait 2–4 weeks after the attack has subsided. * **Drug of Choice (DOC):** * Acute Gout: **NSAIDs** (e.g., Indomethacin, Naproxen). * Acute Gout in Renal Failure: **Corticosteroids**. * Chronic Gout (Overproducers/Underexcretors): **Allopurinol**. * **HLA-B*5801:** Testing is recommended in certain populations before starting Allopurinol to prevent **Stevens-Johnson Syndrome (SJS)**.

Q: All of the following are true about Aspirin except?

It is a reversible inhibitor of COX.. **Explanation** The correct answer is **D**, as Aspirin is an **irreversible** inhibitor of the Cyclooxygenase (COX) enzyme, not a reversible one. **1. Why Option D is the Correct Answer (The Concept):** Aspirin (Acetylsalicylic acid) is unique among NSAIDs because it covalently modifies the COX-1 and COX-2 enzymes by **acetylating a specific serine residue** at the active site. This covalent bond permanently inactivates the enzyme. Since platelets lack a nucleus, they cannot synthesize new proteins; thus, the inhibition lasts for the entire lifespan of the platelet (approx. 8–11 days). **2. Analysis of Other Options:** * **Option A:** At low doses (75–150 mg), Aspirin selectively inhibits COX-1 in platelets, reducing Thromboxane A2 (TXA2) production, which makes it an effective **antiplatelet** agent for cardiovascular prophylaxis. * **Option B:** Because the inhibition is irreversible and platelets cannot regenerate the enzyme, the synthesis of **Thromboxane A2** is halted for the life of the cell. * **Option C:** Niacin (Vitamin B3) causes flushing mediated by **Prostaglandin D2 (PGD2)**. Pre-treatment with Aspirin inhibits COX and prevents the synthesis of these prostaglandins, thereby reducing the flushing side effect. **Clinical Pearls for NEET-PG:** * **Zero-order kinetics:** At high/toxic doses, Aspirin follows zero-order elimination. * **Reye’s Syndrome:** Avoid Aspirin in children with viral infections (Varicella/Influenza) due to the risk of hepatic encephalopathy. * **Aspirin Triad (Samter’s Triad):** Asthma, Nasal polyposis, and Aspirin hypersensitivity. * **Uric Acid:** Low-dose aspirin decreases uric acid excretion (hyperuricemia), while high-dose aspirin is uricosuric.

Q: Icatibant is a?

bradykinin B2 antagonist. ### Explanation **Correct Option: B. Bradykinin B2 antagonist** **Mechanism of Action:** Icatibant is a synthetic decapeptide that acts as a potent and selective **competitive antagonist at the Bradykinin B2 receptor**. Bradykinin is a key mediator in inflammatory processes and vascular permeability. In conditions like **Hereditary Angioedema (HAE)**, there is an overproduction of bradykinin due to C1-esterase inhibitor deficiency. Excessive bradykinin binds to B2 receptors on vascular endothelial cells, leading to massive vasodilation and increased capillary permeability, which results in life-threatening swelling (edema). By blocking the B2 receptor, Icatibant prevents these effects and provides symptomatic relief during acute attacks. **Analysis of Incorrect Options:** * **Option A (B1 antagonist):** B1 receptors are typically "inducible" and upregulated during chronic inflammation or tissue injury. While they play a role in pain, Icatibant does not target them. * **Option C (B3 antagonist):** There is no clinically significant "Bradykinin B3" receptor targeted by current pharmacological agents in this context. * **Option D (H3 antagonist):** Histamine H3 receptors are primarily located in the CNS and regulate neurotransmitter release. Examples include Pitolisant (used for narcolepsy), not Icatibant. **High-Yield Clinical Pearls for NEET-PG:** * **Indication:** Approved for the treatment of **acute attacks of Hereditary Angioedema (HAE)** in adults. * **Route:** Administered via **subcutaneous injection** (usually in the abdomen). * **Key Distinction:** Unlike allergic angioedema, HAE is **bradykinin-mediated**, meaning it does *not* respond to antihistamines or corticosteroids. * **Other HAE Drugs:** * **Ecallantide:** A Kallikrein inhibitor. * **Danazol:** An androgen used for prophylaxis (increases C1-esterase inhibitor levels). * **Lanadelumab:** A monoclonal antibody against plasma kallikrein.

Q: Misoprostol is an analogue of:

PGE1. **Explanation:** **Misoprostol** is a synthetic methyl analogue of **Prostaglandin E1 (PGE1)**. It is primarily used in clinical practice for its cytoprotective effects on the gastric mucosa and its potent oxytocic properties. 1. **Why PGE1 is correct:** Misoprostol mimics the action of endogenous PGE1. In the stomach, it binds to EP3 receptors on parietal cells to inhibit gastric acid secretion and stimulates mucus and bicarbonate secretion. In the uterus, it causes cervical ripening and uterine contractions, making it vital for obstetric and gynecological procedures. 2. **Why other options are incorrect:** * **PGE2 (Dinoprostone):** While also used for cervical ripening, Misoprostol is specifically a PGE1 analogue. Dinoprostone is the naturally occurring PGE2. * **PGF2α (Carboprost/Dinoprost):** These are used to control postpartum hemorrhage (PPH) by causing strong uterine contractions but belong to the F-series of prostaglandins. * **PGI2 (Epoprostenol):** This is Prostacyclin, used primarily as a vasodilator and inhibitor of platelet aggregation in pulmonary arterial hypertension. **High-Yield Clinical Pearls for NEET-PG:** * **NSAID-induced Ulcers:** Misoprostol is the drug of choice for the *prevention* of NSAID-induced gastric ulcers (though PPIs are more commonly used due to better tolerability). * **Obstetric Uses:** Used for medical abortion (combined with Mifepristone), induction of labor, and management of Postpartum Hemorrhage (PPH). * **Side Effects:** The most common side effect is **diarrhea** and abdominal cramps. * **Contraindication:** It is strictly contraindicated in pregnancy unless used for legal termination, as it is highly **teratogenic** (associated with Moebius syndrome).

Q: Infliximab is:

An IgG1 chimeric monoclonal antibody against TNF α. **Explanation:** **Infliximab** is a potent biological agent used in the management of autoimmune conditions like Rheumatoid Arthritis, Crohn’s disease, and Psoriasis. 1. **Why Option A is Correct:** Infliximab is a **chimeric** monoclonal antibody. In pharmacology, "chimeric" means it is composed of a combination of mouse (murine) variable regions (~25%) and human constant regions (~75%). It belongs to the **IgG1** subclass and works by binding with high affinity to both soluble and transmembrane forms of **TNF-α**, neutralizing its pro-inflammatory effects. 2. **Why Other Options are Incorrect:** * **Option B:** **Adalimumab** and **Golimumab** are examples of **fully human** monoclonal antibodies against TNF-α. They are preferred in some cases because they have lower immunogenicity compared to chimeric antibodies. * **Option C:** **Etanercept** is the **P75 TNF receptor fusion protein**. It acts as a "decoy receptor" that binds to TNF molecules in the circulation, preventing them from interacting with cell surface receptors. **High-Yield Clinical Pearls for NEET-PG:** * **Nomenclature Hack:** The suffix **"-ximab"** denotes a **chi**meric antibody (e.g., Infliximab, Rituximab), while **"-umab"** denotes a fully h**uma**n antibody (e.g., Adalimumab). * **Pre-treatment Screening:** Before starting any TNF-α inhibitor, patients **must** be screened for **Latent Tuberculosis** (via TST or IGRA) and Hepatitis B, as these drugs can cause reactivation of these infections. * **Adverse Effects:** Increased risk of serious infections, lymphoma, and worsening of congestive heart failure (CHF).

Question 1

Which of the following analgesic combinations should be avoided?

Accepted Answer

Ibuprofen and Diclofenac

Answer

Aspirin and Codeine

Answer

Paracetamol and Dextropropoxyphene

Answer

Ibuprofen and Paracetamol

Question 2

Which NSAID is proposed to act by inhibition of COX-3?

Accepted Answer

Paracetamol

Answer

Nimesulide

Answer

Ketorolac

Answer

Rofecoxib

Question 3

Which among the following drugs is contraindicated in renal failure?

Accepted Answer

Pethidine

Answer

Morphine

Answer

Fentanyl

Answer

Atracurium

Question 4

Aspirin is associated with which of the following conditions?

Accepted Answer

Reye's Syndrome

Answer

Sjogren Syndrome

Answer

Reiter Syndrome

Answer

None of the above

Question 5

Acute gouty arthritis is seen early following treatment with which of the following medications?

Accepted Answer

Allopurinol

Answer

Rasburicase

Answer

Probenecid

Answer

Sulfinpyrazone

Question 6

All of the following are true about Aspirin except?

Accepted Answer

It is a reversible inhibitor of COX.

Answer

At low doses it acts as an antiplatelet drug.

Answer

It irreversibly inhibits the synthesis of Thromboxane.

Answer

It is used to inhibit Niacin induced flushing.

Question 7

Icatibant is a?

Accepted Answer

bradykinin B2 antagonist

Answer

bradykinin B1 antagonist

Answer

bradykinin B3 antagonist

Answer

histamine receptor H3 antagonist

Question 8

Which of the following is NOT a feature of morphine withdrawal?

Accepted Answer

Diarrhea

Answer

Piloerection

Answer

Insomnia

Answer

Rhinorrhea

Question 9

Misoprostol is an analogue of:

Accepted Answer

PGE1

Answer

PGE2

Answer

PGF2

Answer

PGI2

Question 10

Infliximab is:

Accepted Answer

An IgG1 chimeric monoclonal antibody against TNF α

Answer

An IgG1 fully human monoclonal antibody against TNF α

Answer

A P75 TNF receptor fusion protein

Answer

None of the above

Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs — MCQs

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