Analgesics and Anti-inflammatory Drugs Practice Questions

Q: A patient with malignancy is experiencing severe pain. Which of the following opioid analgesics can be administered via a transdermal patch for pain relief?

Fentanyl. ### Explanation **Correct Option: C. Fentanyl** Fentanyl is a potent synthetic opioid agonist (approximately 80–100 times more potent than morphine). Its high **lipid solubility** and **low molecular weight** make it the ideal candidate for transdermal delivery [1]. The transdermal patch (Duragesic) provides a stable, continuous release of the drug over 72 hours, making it a gold-standard choice for managing chronic, stable malignant pain in patients who have difficulty swallowing or require long-term analgesia. **Analysis of Incorrect Options:** * **A. Morphine:** While it is the standard for cancer pain (WHO Step 3), it is relatively hydrophilic (low lipid solubility) [1]. This makes it unsuitable for effective absorption through the skin via a simple patch [2]. It is typically administered orally or intravenously. * **B. Pentazocine:** This is an opioid agonist-antagonist. It is not available in transdermal form and is generally avoided in severe malignancy pain because it has a "ceiling effect" on analgesia and can precipitate withdrawal in patients already on pure mu-agonists. * **D. Tramadol:** A weak mu-agonist and SNRI, used for moderate pain (WHO Step 2). It is administered orally or parenterally, but not via a transdermal patch. **High-Yield Clinical Pearls for NEET-PG:** * **Buprenorphine** is the only other opioid commonly used in transdermal patches (often used in chronic non-malignant pain). * **Fentanyl Patch Caution:** It is **not** for acute or postoperative pain because it takes 12–24 hours to reach therapeutic plasma concentrations. * **Fentanyl Metabolism:** It is metabolized by **CYP3A4**; inhibitors of this enzyme can increase fentanyl toxicity. * **Side Effects:** Like all opioids, it causes constipation and respiratory depression, but it is less likely to cause histamine release compared to morphine.

Q: All of the following are true regarding Ketorolac, EXCEPT?

Respiratory depression is a side effect.. **Explanation:** **Ketorolac** is a potent Non-Steroidal Anti-inflammatory Drug (NSAID) belonging to the pyrrolo-pyrrole group. It is unique because its analgesic efficacy is comparable to low-dose morphine, yet it lacks the side-effect profile of opioids. 1. **Why Option A is the Correct Answer (The False Statement):** Unlike opioids (e.g., Morphine), Ketorolac does **not** cause respiratory depression, sedation, or miosis. It acts by inhibiting cyclooxygenase (COX) enzymes to reduce prostaglandin synthesis, a mechanism that does not involve the brainstem respiratory centers. Therefore, respiratory depression is not a side effect of Ketorolac. 2. **Analysis of Other Options:** * **Option B:** Ketorolac is significantly **more potent than Aspirin**. While Aspirin is used for mild pain, Ketorolac is used for moderate-to-severe acute pain. * **Option C:** The **duration of action** is approximately **4–6 hours**, necessitating dosing every 6 hours when used for acute pain management. * **Option D:** It is **primarily used as an analgesic**, especially in post-operative settings. While it has anti-inflammatory properties, its systemic use is limited by its high risk of gastrointestinal toxicity and renal impairment if used long-term. **High-Yield Clinical Pearls for NEET-PG:** * **The "5-Day Rule":** Systemic Ketorolac (IM/IV/Oral) should not be used for more than **5 days** due to the high risk of peptic ulceration and renal failure. * **Opioid Sparing Effect:** It is frequently used in post-operative care to reduce the requirement for opioids. * **Topical Use:** Ketorolac 0.5% ophthalmic solution is commonly used to treat seasonal allergic conjunctivitis and post-operative ocular inflammation. * **Contraindication:** Avoid in patients with "Aspirin Triad" (Asthma, Nasal polyps, NSAID sensitivity).

Q: Which uricosuric agent is used for acute gout in a patient with chronic renal failure?

Benzbromarone. ### Explanation **Correct Answer: C. Benzbromarone** **Why Benzbromarone is correct:** Benzbromarone is a potent uricosuric agent that inhibits the URAT1 transporter in the proximal tubule, increasing uric acid excretion. Unlike other uricosurics, it is unique because it **retains its efficacy in patients with moderate-to-severe chronic renal failure (CRF)**, even when the Glomerular Filtration Rate (GFR) is as low as 20 ml/min. While it is primarily used for chronic management, it is the preferred uricosuric choice in the context of renal impairment. **Analysis of Incorrect Options:** * **A. Probenecid:** This is a classic uricosuric, but it **loses efficacy** when the GFR falls below 50–60 ml/min. Therefore, it is ineffective in patients with significant chronic renal failure. * **B. Colchicine:** While colchicine is a first-line drug for *acute* gout attacks, it is **not a uricosuric agent** (it does not increase uric acid excretion). Furthermore, its dose must be strictly reduced in renal failure to avoid toxicity (neuromyopathy). * **C. Aspirin:** In low doses, aspirin actually **inhibits** uric acid excretion (causing hyperuricemia) and is contraindicated in gout. High-dose aspirin is uricosuric but is rarely used due to toxicity. **High-Yield NEET-PG Pearls:** 1. **Uricosuric of Choice in Renal Failure:** Benzbromarone (effective down to GFR 20 ml/min). 2. **The "Aspirin Paradox":** Low-dose aspirin (1–2g/day) causes uric acid retention; high-dose aspirin (>5g/day) is uricosuric. 3. **Lesinurad:** A newer URAT1 inhibitor used as adjunct therapy with Xanthine Oxidase Inhibitors. 4. **Hepatotoxicity:** The main clinical concern with Benzbromarone is potential hepatotoxicity, requiring periodic liver function monitoring.

Q: Which of the following statements is false regarding Leflunomide?

Acts by inhibiting IMP dehydrogenase enzyme.. ### Explanation **Leflunomide** is a Disease-Modifying Antirheumatic Drug (DMARD) used primarily in the management of Rheumatoid Arthritis. **Why Option B is the correct (False) statement:** Leflunomide is a prodrug that is converted into its active metabolite, **A77 1726 (Teriflunomide)**. This metabolite acts by inhibiting **Dihydroorotate Dehydrogenase (DHODH)**, a key mitochondrial enzyme in the *de novo* pyrimidine synthesis pathway. It does **not** inhibit IMP dehydrogenase; IMP dehydrogenase is the target of **Mycophenolate Mofetil**, which inhibits *de novo* purine synthesis. **Analysis of other options:** * **Option A:** It is a first-line DMARD used for **Rheumatoid Arthritis**, often as an alternative to Methotrexate. * **Option C:** By inhibiting pyrimidine synthesis, it arrests the cell cycle in the G1 phase. Since T and B lymphocytes rely heavily on *de novo* synthesis for expansion, it effectively **inhibits the proliferation of T and B cells**, exerting an immunosuppressive effect. * **Option D:** Leflunomide is highly **teratogenic** and is contraindicated in pregnancy (Pregnancy Category X). Due to its long half-life (approx. 2 weeks), a "Cholestyramine washout" procedure is required to rapidly clear the drug from the body if a patient wishes to become pregnant. ### High-Yield Clinical Pearls for NEET-PG: * **Mechanism:** Inhibits Dihydroorotate Dehydrogenase → ↓ Pyrimidine synthesis. * **Side Effects:** Hepatotoxicity (monitor LFTs), diarrhea, hypertension, and alopecia. * **Washout:** Cholestyramine is used to enhance fecal excretion because the drug undergoes extensive enterohepatic circulation. * **Comparison:** Remember: **L**eflunomide = **P**yrimidines; **M**ycophenolate = **P**urines.

Q: Which of the following opioid analgesics is most likely to cause central nervous system (CNS) disturbance?

meperidine. The correct answer is **Meperidine** (also known as Pethidine). The primary reason for its association with CNS disturbances lies in its metabolism [3], [4]. 1. **Why Meperidine is correct:** Meperidine is metabolized in the liver by N-demethylation to **normeperidine**, an active metabolite [3]. Unlike meperidine, which is a sedative, normeperidine is a potent **CNS stimulant**. It has a longer half-life (15–20 hours) and accumulates, especially in patients with renal impairment [4]. Accumulation leads to CNS hyperexcitability, manifesting as tremors, muscle twitches, hyperreflexia, and **seizures** [4]. 2. **Why other options are incorrect:** * **Morphine:** While it can cause sedation and respiratory depression, its primary metabolites (Morphine-6-glucuronide) are mainly associated with analgesia and respiratory effects, not CNS excitation/seizures. * **Heroin (Diacetylmorphine):** A highly lipid-soluble prodrug that rapidly converts to morphine in the brain [1]. Its side effect profile mirrors morphine but with higher addiction potential. * **Fentanyl:** A potent synthetic opioid used in anesthesia. It is known for cardiovascular stability and lacks the excitatory metabolites seen with meperidine. **NEET-PG High-Yield Pearls:** * **Serotonin Syndrome:** Meperidine inhibits the reuptake of serotonin. It is strictly contraindicated with **MAO Inhibitors**, as the combination can trigger a fatal hyperpyrexic coma or serotonin syndrome [2]. * **Mydriasis:** Unlike most opioids that cause "pinpoint pupils" (miosis), meperidine can cause **mydriasis** due to its atropine-like (antimuscarinic) structural properties [4]. * **Clinical Use:** It is specifically indicated for **shivering** (post-operative or drug-induced) but is no longer preferred for chronic pain due to metabolite toxicity [4].

Q: Which of the following statements about drugs used in rheumatoid arthritis is false?

Tofacitinib is given intravenously. ### Explanation The correct answer is **C (Tofacitinib is given intravenously)** because it is a false statement. **1. Why Option C is the correct answer (False statement):** Tofacitinib is a **Janus Kinase (JAK) inhibitor**, categorized as a "Targeted Synthetic DMARD" (tsDMARD). Unlike biological DMARDs (which are proteins/monoclonal antibodies and must be injected), Tofacitinib is a small molecule drug. Its primary clinical advantage is that it is **administered orally** (usually 5 mg twice daily), not intravenously. **2. Analysis of other options:** * **Option A (True):** Tofacitinib is a non-selective JAK inhibitor that primarily inhibits **JAK1 and JAK3**, and to a lesser extent JAK2. This blocks the signaling pathway for various cytokines involved in lymphocyte activation. * **Option B (True):** **Tocilizumab** is a recombinant humanized monoclonal antibody that acts as an **IL-6 receptor antagonist**. IL-6 is a key pro-inflammatory cytokine in the pathogenesis of Rheumatoid Arthritis (RA). * **Option D (True):** Tocilizumab is versatile in its administration; it can be given as an **intravenous (IV) infusion** (usually monthly) or as a **subcutaneous (SC) injection** (usually weekly). **3. High-Yield Clinical Pearls for NEET-PG:** * **JAK Inhibitors:** Other examples include Baricitinib (JAK1/2) and Upadacitinib (JAK1 selective). All are **oral**. * **Pre-treatment Screening:** Before starting Tofacitinib or Biologics, always screen for **Latent TB** (using Mantoux or IGRA) and Hepatitis B/C, as these drugs can cause reactivation. * **Adverse Effects of Tofacitinib:** Increased risk of serious infections, herpes zoster reactivation, and changes in lipid profiles (increased LDL/HDL). * **IL-1 Inhibitor:** Anakinra (not to be confused with IL-6 inhibitors).

Q: All the following drugs are reversible inhibitors of COX EXCEPT?

Aspirin. ### Explanation **Correct Answer: C. Aspirin** **Mechanism of Action:** The core concept here is the nature of the chemical bond formed between the drug and the enzyme Cyclooxygenase (COX). Most Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) bind to the active site of COX via non-covalent interactions, making them **reversible inhibitors**. **Aspirin (Acetylsalicylic acid)** is unique because it **irreversibly** inhibits COX-1 and COX-2. It achieves this by covalently attaching an acetyl group to a specific serine residue (Serine 529 in COX-1 and Serine 516 in COX-2) near the active site. This permanent modification physically blocks the channel, preventing arachidonic acid from reaching the catalytic site. The enzyme remains inactive for its entire lifespan; recovery of function requires the synthesis of new enzyme molecules. **Analysis of Incorrect Options:** * **A. Diclofenac:** A potent phenylacetic acid derivative that acts as a competitive, reversible inhibitor of COX. * **B. Ibuprofen:** A propionic acid derivative that reversibly competes with arachidonic acid for the COX binding site. * **D. Indomethacin:** An indole derivative and a powerful reversible inhibitor of COX, often used for closing a Patent Ductus Arteriosus (PDA). **High-Yield Clinical Pearls for NEET-PG:** * **Antiplatelet Effect:** Because platelets lack a nucleus, they cannot synthesize new COX enzymes. A single low dose of Aspirin inhibits platelet COX-1 for the remainder of the platelet's life (7–10 days), explaining its use in cardiovascular prophylaxis. * **Zero-Order Kinetics:** At high/toxic doses, Aspirin metabolism shifts from first-order to zero-order kinetics. * **Reye’s Syndrome:** Aspirin is contraindicated in children with viral infections (e.g., influenza, varicella) due to the risk of fulminant hepatic failure and encephalopathy. * **Aspirin Triad (Samter’s Triad):** Asthma, Nasal polyposis, and Aspirin hypersensitivity.

Question 1

The anti-inflammatory action of corticosteroids is due to blocking of which of the following?

Accepted Answer

Breakdown of phospholipids

Answer

15-lipoxygenase

Answer

Prostaglandin synthetase

Answer

Thromboxane synthetase

Question 2

A patient with malignancy is experiencing severe pain. Which of the following opioid analgesics can be administered via a transdermal patch for pain relief?

Accepted Answer

Fentanyl

Answer

Morphine

Answer

Pentazocine

Answer

Tramadol

Question 3

All of the following are true regarding Ketorolac, EXCEPT?

Accepted Answer

Respiratory depression is a side effect.

Answer

It is more potent than Aspirin.

Answer

Its duration of action (VA) is 5-6 hours.

Answer

It is primarily used as an analgesic.

Question 4

Which uricosuric agent is used for acute gout in a patient with chronic renal failure?

Accepted Answer

Benzbromarone

Answer

Probenecid

Answer

Colchicine

Answer

Aspirin

Question 5

Which of the following statements is false regarding Leflunomide?

Accepted Answer

Acts by inhibiting IMP dehydrogenase enzyme.

Answer

Used in the treatment of Rheumatoid arthritis.

Answer

Inhibits proliferation of T and B cells.

Answer

It is contraindicated in pregnancy.

Question 6

A patient presents with severe shortness of breath whenever they take aspirin for a headache. Which of the following is most likely responsible for this effect?

Accepted Answer

Leukotrienes

Answer

Prostaglandin E

Answer

Thromboxane A2

Answer

Prostacyclin

Question 7

Which of the following opioid analgesics is most likely to cause central nervous system (CNS) disturbance?

Accepted Answer

meperidine

Answer

heroin

Answer

morphine

Answer

fentanyl

Question 8

Glucocorticoids act in inflammation by inhibiting which of the following?

Accepted Answer

Lipocortin

Answer

Interleukin-2

Answer

C-reactive protein

Question 9

Which of the following statements about drugs used in rheumatoid arthritis is false?

Accepted Answer

Tofacitinib is given intravenously

Answer

Tofacitinib inhibits JAK1 and JAK3

Answer

Tocilizumab inhibits IL-6

Answer

Tocilizumab is given by intravenous and subcutaneous routes

Question 10

All the following drugs are reversible inhibitors of COX EXCEPT?

Accepted Answer

Aspirin

Answer

Diclofenac

Answer

Ibuprofen

Answer

Indomethacin

Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs — MCQs

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