Analgesics and Anti-inflammatory Drugs Practice Questions

Q: Which one of the following drugs is NOT a non-opioid analgesic?

Methadone. **Explanation:** The classification of analgesics is a high-yield topic for NEET-PG. Analgesics are broadly divided into two categories: **Non-opioids** (NSAIDs and Acetaminophen) and **Opioids** (Narcotics). **Why Methadone is the correct answer:** **Methadone** is a potent **synthetic opioid agonist** that acts primarily on $\mu$-opioid receptors. Unlike NSAIDs, it does not inhibit cyclooxygenase (COX) enzymes. It is clinically unique because it also acts as an NMDA receptor antagonist and inhibits the reuptake of serotonin and norepinephrine. It is primarily used for detoxification and maintenance treatment of opioid abstinence syndromes (heroin addiction) and for chronic pain management due to its long half-life. **Why the other options are incorrect:** * **Meloxicam:** A selective **COX-2 inhibitor** belonging to the oxicam class of NSAIDs. It is a classic non-opioid analgesic used for osteoarthritis and rheumatoid arthritis. * **Nimesulide:** A preferential **COX-2 inhibitor**. It is a non-opioid analgesic frequently used for acute pain, though its use is restricted in some regions due to potential hepatotoxicity. * **Nabumetone:** A **non-acidic NSAID** (prodrug) that is converted into its active metabolite in the liver. It is a non-opioid analgesic known for having a lower incidence of GI side effects compared to traditional NSAIDs. **NEET-PG High-Yield Pearls:** * **Methadone's Half-life:** It has a very long and variable half-life (15–60 hours), which can lead to cumulative toxicity. * **NMDA Antagonism:** Methadone’s ability to block NMDA receptors makes it effective for neuropathic pain where other opioids might fail. * **EKG Monitoring:** Methadone is notorious for causing **QT interval prolongation** and *Torsades de Pointes*; baseline EKG is recommended.

Q: Ibuprofen is contraindicated in which of the following patient groups?

Patients with asthma. Explanation: The correct answer is **B. Patients with asthma**. **Mechanism of Action:** Ibuprofen is a non-selective Non-Steroidal Anti-Inflammatory Drug (NSAID) that inhibits the enzyme **Cyclooxygenase (COX)** [2]. In the body, Arachidonic acid is metabolized via two main pathways: the COX pathway (producing prostaglandins) and the **Lipoxygenase (LOX) pathway** (producing leukotrienes). When NSAIDs like Ibuprofen inhibit the COX pathway, the metabolism of Arachidonic acid is "shunted" toward the LOX pathway. This leads to an overproduction of **Cysteinyl Leukotrienes (LTC4, LTD4, LTE4)**, which are potent bronchoconstrictors [3]. In susceptible individuals, this triggers **NSAID-Exacerbated Respiratory Disease (NERD)**, characterized by bronchospasm, airway inflammation, and rhinitis. **Analysis of Incorrect Options:** * **A. Fever:** Ibuprofen is an effective antipyretic and is commonly used to treat fever. * **C. Amoebic Dysentery:** This is an intestinal infection caused by *E. histolytica*. While NSAIDs are generally avoided in severe GI inflammation due to gastric irritation [1], there is no specific contraindication related to the pathology of amoebiasis. * **D. Bronchitis:** This is an inflammation of the bronchial tubes (often viral). Unlike asthma, it does not typically involve the leukotriene-sensitive hyperreactivity that leads to NSAID-induced bronchospasm. **High-Yield Clinical Pearls for NEET-PG:** * **Samter’s Triad (Aspirin-Exacerbated Respiratory Disease):** Consists of Asthma, Aspirin sensitivity, and Nasal polyps. * **Safe Alternative:** **Paracetamol (Acetaminophen)** is generally considered the analgesic of choice in asthmatic patients as it is a weak peripheral COX inhibitor [2]. * **Other Contraindications for NSAIDs:** Peptic ulcer disease, chronic kidney disease (CKD), and severe heart failure [1].

Q: Which of the following is an injectable COX-2 inhibitor?

Parecoxib. **Explanation:** **Parecoxib** is the correct answer because it is a **prodrug of Valdecoxib** and is currently the only selective COX-2 inhibitor available for **parenteral (injectable)** administration. It is rapidly converted by liver enzymes into its active form, Valdecoxib. It is primarily used in hospital settings for the short-term management of acute postoperative pain when oral medication is not feasible. **Analysis of Incorrect Options:** * **Celecoxib (Option A):** This is the prototype selective COX-2 inhibitor. It is administered strictly via the **oral route** and is commonly used for chronic conditions like osteoarthritis and rheumatoid arthritis. * **Etoricoxib (Option B):** This is a second-generation selective COX-2 inhibitor with a long half-life, allowing for once-daily dosing. Like Celecoxib, it is only available in **oral formulations**. * **None of the above (Option D):** This is incorrect as Parecoxib serves as the specific injectable representative of this class. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Selective COX-2 inhibitors lack the anti-platelet effects of non-selective NSAIDs (as they do not inhibit COX-1/TXA2) and carry a lower risk of GI ulcers. * **Contraindication:** All selective COX-2 inhibitors (including Parecoxib) are contraindicated in patients with **Ischemic Heart Disease (IHD)** or stroke due to an increased risk of thrombotic cardiovascular events. * **Sulfonamide Allergy:** Celecoxib contains a sulfonamide moiety; use caution in patients with sulfa allergies. * **Rofecoxib/Valdecoxib:** These were withdrawn globally due to high cardiovascular toxicity.

Q: A widely used drug that suppresses cellular immunity, inhibits prostaglandin and leukotriene synthesis, and increases the catabolism of IgG antibody is:

Prednisone. ### Explanation **Correct Option: B. Prednisone** Prednisone is a corticosteroid that exerts broad immunosuppressive and anti-inflammatory effects through multiple mechanisms: 1. **Suppression of Cellular Immunity:** It inhibits the production of IL-2 and other cytokines, leading to decreased T-cell proliferation. 2. **Inhibition of Prostaglandins and Leukotrienes:** Glucocorticoids induce **Annexin-1 (Lipocortin-1)**, which inhibits **Phospholipase A2**. This blocks the release of arachidonic acid, effectively shutting down both the cyclooxygenase (COX) and lipoxygenase (LOX) pathways. 3. **IgG Catabolism:** High doses of steroids increase the fractional catabolic rate of IgG, reducing its serum concentration—a property utilized in treating autoimmune conditions like ITP. --- ### Why Other Options are Incorrect: * **A. Cyclophosphamide:** An alkylating agent that cross-links DNA. While it suppresses B-cell and T-cell function, it does not directly inhibit Phospholipase A2 or the synthesis of prostaglandins/leukotrienes. * **C. Cyclosporine:** A calcineurin inhibitor that specifically inhibits IL-2 production. It focuses on T-cell suppression but does not affect the arachidonic acid cascade or IgG catabolism. * **D. Infliximab:** A monoclonal antibody that neutralizes **TNF-α**. It is a targeted biologic and does not possess the broad metabolic or phospholipase-inhibiting effects of steroids. --- ### NEET-PG High-Yield Pearls: * **Mechanism Focus:** Steroids inhibit **Phospholipase A2** (upstream), whereas NSAIDs only inhibit **COX** (downstream). * **Hematologic Effect:** Steroids cause **"Neutrophilic Leukocytosis"** (due to demargination) but cause lymphopenia, eosinopenia, and monocytopenia. * **Metabolic Effect:** They are catabolic in nature (muscle wasting, bone loss) but cause truncal obesity due to insulin antagonism and redistribution of fat.

Q: Which of the following drugs inhibits an enzyme in prostaglandin synthesis?

Aspirin. **Explanation:** The correct answer is **B. Aspirin**. **Mechanism of Action:** Aspirin (Acetylsalicylic acid) is a Non-Steroidal Anti-Inflammatory Drug (NSAID) that acts by **irreversibly inhibiting the Cyclooxygenase (COX-1 and COX-2) enzymes**. It achieves this by acetylating a specific serine residue at the active site of the enzyme. This inhibition prevents the conversion of arachidonic acid into Prostaglandin $H_2$ ($PGH_2$), the precursor for prostaglandins, prostacyclin, and thromboxane $A_2$. **Analysis of Incorrect Options:** * **A. Aminocaproic acid:** This is an **antifibrinolytic** agent. It inhibits plasminogen activation and plasmin activity, used to control bleeding. * **C. Aprotinin:** A natural protease inhibitor that acts as an **antifibrinolytic** by inhibiting plasmin and kallikrein. * **D. Alteplase:** A recombinant tissue plasminogen activator (**tPA**). It is a **thrombolytic** drug that converts plasminogen to plasmin to dissolve existing blood clots. **High-Yield NEET-PG Pearls:** * **Irreversibility:** Aspirin is the only NSAID that inhibits COX enzymes **irreversibly**. All other NSAIDs (like Ibuprofen) are reversible inhibitors. * **Antiplatelet Effect:** Because platelets cannot synthesize new proteins, aspirin-induced COX-1 inhibition lasts for the entire lifespan of the platelet (approx. 7–10 days). * **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 (influenza/varicella) due to the risk of fulminant hepatic failure and encephalopathy.

Q: All of the following statements are true except?

Cyclooxygenase-I (COX-I) is an inducible enzyme.. ### Explanation The correct answer is **B**, as Cyclooxygenase-I (COX-1) is a **constitutive** enzyme, not an inducible one. **1. Why Option B is the Correct Answer (The False Statement):** In the arachidonic acid cascade, COX enzymes exist in two primary isoforms. **COX-1** is "constitutive," meaning it is expressed constantly in most tissues (e.g., stomach lining, kidneys, and platelets). It serves "housekeeping" functions like gastric cytoprotection and maintaining renal blood flow. In contrast, **COX-2** is the "inducible" isoform, synthesized primarily in response to inflammatory stimuli, cytokines, and growth factors. **2. Analysis of Other Options:** * **Option A:** True. Arachidonic acid, released from membrane phospholipids by Phospholipase A2, serves as the common precursor for both prostaglandins (via the COX pathway) and leukotrienes (via the LOX pathway). * **Option C:** True. COX-2 expression is triggered at sites of injury by pro-inflammatory mediators like Interleukin-1 (IL-1) and Tumor Necrosis Factor (TNF). * **Option D:** True. Cysteinyl leukotrienes (LTC4, LTD4, LTE4) are potent bronchoconstrictors and are significantly more powerful than histamine in inducing airway smooth muscle contraction. **3. NEET-PG High-Yield Clinical Pearls:** * **Aspirin:** Irreversibly inhibits COX-1 and COX-2 via acetylation. * **Selective COX-2 Inhibitors (e.g., Celecoxib):** Provide anti-inflammatory effects with a lower risk of gastric ulcers but carry an increased risk of cardiovascular events (due to inhibition of PGI2 without affecting TXA2). * **Platelets:** Contain only COX-1; since they lack a nucleus, they cannot regenerate the enzyme once inhibited. * **Glucocorticoids:** Inhibit inflammation by inducing *annexins*, which inhibit Phospholipase A2, and by repressing the expression of COX-2.

Q: Which monoclonal antibody is used for Muckle-Wells syndrome?

Canakinumab. **Explanation:** **Canakinumab** is the correct answer because it is a high-affinity human monoclonal antibody targeted against **Interleukin-1 beta (IL-1β)**. Muckle-Wells Syndrome is part of a group of rare autoinflammatory diseases known as **Cryopyrin-Associated Periodic Syndromes (CAPS)**. These conditions are caused by mutations in the *NLRP3* gene, leading to overactivation of the inflammasome and excessive production of IL-1β. By neutralizing IL-1β, Canakinumab effectively controls the systemic inflammation associated with this syndrome. **Analysis of Incorrect Options:** * **Catumaxomab:** A trifunctional rat-mouse hybrid monoclonal antibody that targets **EpCAM** and **CD3**. It is primarily used for the treatment of malignant ascites in patients with EpCAM-positive carcinomas. * **Certolizumab (Ceolizumab):** A PEGylated Fab' fragment of a humanized TNF-inhibitor. It is used for inflammatory conditions like Rheumatoid Arthritis and Crohn’s disease, but it does not target the IL-1 pathway required for CAPS. * **Cetuximab:** A monoclonal antibody that inhibits the **Epidermal Growth Factor Receptor (EGFR)**. It is used in the treatment of metastatic colorectal cancer and head and neck squamous cell carcinoma. **High-Yield Clinical Pearls for NEET-PG:** * **IL-1 Inhibitors Trio:** Remember **Anakinra** (IL-1 receptor antagonist), **Rilonacept** (IL-1 trap), and **Canakinumab** (anti-IL-1β mAb) as the primary treatments for CAPS and refractory Gout. * **Muckle-Wells Syndrome Triad:** Characterized by recurrent urticaria-like skin rash, progressive sensorineural deafness, and secondary amyloidosis. * **Canakinumab** is also FDA-approved for Systemic Juvenile Idiopathic Arthritis (sJIA).

Q: Etanercept is a biological disease-modifying agent used in the management of rheumatoid arthritis. What is its mechanism of action?

TNF alpha blockade. ### Explanation **Correct Option: A. TNF alpha blockade** Etanercept is a biological Disease-Modifying Anti-Rheumatic Drug (bDMARD). It is a **soluble decoy receptor** consisting of two extracellular domains of the human TNF receptor (p75) fused to the Fc portion of human IgG1. It works by binding to both **TNF-α** and **TNF-β** (lymphotoxin-alpha) in the circulation, preventing them from interacting with cell-surface receptors. This neutralizes the pro-inflammatory cascade responsible for joint destruction in rheumatoid arthritis. **Analysis of Incorrect Options:** * **B. COX-2 inhibition:** This is the mechanism of NSAIDs like Celecoxib and Etoricoxib. While they provide symptomatic relief by reducing prostaglandin synthesis, they do not modify the disease progression. * **C. IL-6 inhibition:** This describes **Tocilizumab** and **Sarilumab**. These agents target the IL-6 receptor rather than TNF. * **D. Stabilization of mast cells:** This is the mechanism of drugs like Sodium Cromoglycate and Ketotifen, used primarily in the management of asthma and allergic rhinitis. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** Remember **"Etanercept intercepts TNF"** (it acts as a decoy). * **Screening:** Before starting any TNF inhibitor (Etanercept, Infliximab, Adalimumab), patients must be screened for **Latent Tuberculosis** (using PPD or IGRA) because TNF is essential for granuloma maintenance. * **Other Indications:** Apart from RA, it is used in Psoriatic Arthritis and Ankylosing Spondylitis. * **Distinction:** Unlike Infliximab (a monoclonal antibody), Etanercept is a **fusion protein**.

Q: Allopurinol potentiates the action of which of the following drugs?

6-Mercaptopurine. **Explanation:** The correct answer is **6-Mercaptopurine (6-MP)**. **Mechanism of Interaction:** Allopurinol is a potent **xanthine oxidase (XO) inhibitor**. 6-Mercaptopurine (an immunosuppressant and anticancer drug) and its prodrug, Azathioprine, are primarily metabolized and inactivated by the enzyme xanthine oxidase into 8-thiouric acid. When Allopurinol is co-administered, it inhibits xanthine oxidase, thereby preventing the degradation of 6-MP. This leads to significantly increased plasma levels of 6-MP, potentiating both its therapeutic effects and its toxicity (especially life-threatening bone marrow suppression). **Analysis of Incorrect Options:** * **A. Corticosteroids:** There is no significant metabolic interaction between Allopurinol and steroids. However, they are often used together in acute gout flares. * **B. Probenecid:** Probenecid is a uricosuric agent. While it can be used with Allopurinol, it actually *increases* the excretion of Alloxanthine (the active metabolite of Allopurinol), potentially requiring a dose adjustment of Allopurinol, rather than being potentiated by it. * **D. Ampicillin:** Allopurinol does not potentiate the action of Ampicillin; however, their co-administration is clinically significant because it markedly increases the incidence of **skin rashes**. **High-Yield Clinical Pearls for NEET-PG:** * **Dose Reduction Rule:** If Allopurinol must be given with 6-Mercaptopurine or Azathioprine, the dose of the latter drugs should be reduced to **1/4th (25%)** of the original dose to avoid toxicity. * **Active Metabolite:** Allopurinol is a prodrug converted by xanthine oxidase into **Alloxanthine (Oxypurinol)**, which acts as a non-competitive suicide inhibitor of the enzyme. * **HLA Association:** Allopurinol is associated with severe cutaneous adverse reactions (SCAR) like Stevens-Johnson Syndrome, particularly in patients with the **HLA-B*5801** allele.

Q: The analgesic effect of Paracetamol is mediated by which receptor?

TRPV1. **Explanation:** Paracetamol (Acetaminophen) is a unique analgesic whose mechanism of action has long been debated. While it is known to inhibit COX enzymes (specifically COX-3 in the CNS), its primary analgesic effect is increasingly attributed to its active metabolite, **AM404**. 1. **Why TRPV1 is correct:** After administration, paracetamol is metabolized in the brain by FAAH (Fatty Acid Amide Hydrolase) into **AM404**. This metabolite acts as a potent agonist at the **Transient Receptor Potential Vanilloid 1 (TRPV1)** receptors in the dorsal horn of the spinal cord. Chronic or over-stimulation of these receptors leads to their desensitization, effectively "shunting" pain signals and providing analgesia. AM404 also inhibits the reuptake of endogenous cannabinoids (Anandamide), further enhancing pain relief. 2. **Analysis of Incorrect Options:** * **NK 1 (Neurokinin 1):** These are receptors for Substance P. Antagonists (like Aprepitant) are used as anti-emetics, not for paracetamol-mediated analgesia. * **BK1 (Bradykinin 1):** Bradykinin is a potent pain mediator; however, paracetamol does not exert its primary effect through BK receptor modulation. * **Px23:** This is not a recognized receptor involved in standard analgesic pharmacology. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Action:** Paracetamol is primarily a **central** analgesic with negligible peripheral anti-inflammatory activity (due to its inactivation by peroxides in inflamed tissues). * **Drug of Choice:** It is the preferred analgesic in children (to avoid Reye’s syndrome) and in patients with peptic ulcers or bleeding disorders. * **Toxicity:** Overdose leads to **Centrilobular Hepatic Necrosis** due to the metabolite **NAPQI**. * **Antidote:** **N-acetylcysteine (NAC)**, which replenishes glutathione stores.

Question 1

Which one of the following drugs is NOT a non-opioid analgesic?

Accepted Answer

Methadone

Answer

Meloxicam

Answer

Nimesulide

Answer

Nabumetone

Question 2

Ibuprofen is contraindicated in which of the following patient groups?

Accepted Answer

Patients with asthma

Answer

Patients with fever

Answer

Patients with amoebic dysentery

Answer

Patients with bronchitis

Question 3

Which of the following is an injectable COX-2 inhibitor?

Accepted Answer

Parecoxib

Answer

Celecoxib

Answer

Etoricoxib

Answer

None of the above

Question 4

A widely used drug that suppresses cellular immunity, inhibits prostaglandin and leukotriene synthesis, and increases the catabolism of IgG antibody is:

Accepted Answer

Prednisone

Answer

Cyclophosphamide

Answer

Cyclosporine

Answer

Infliximab

Question 5

Which of the following drugs inhibits an enzyme in prostaglandin synthesis?

Accepted Answer

Aspirin

Answer

Aminocaproic acid

Answer

Aprotinin

Answer

Alteplase

Question 6

All of the following statements are true except?

Accepted Answer

Cyclooxygenase-I (COX-I) is an inducible enzyme.

Answer

Prostaglandins and leukotrienes are derived from arachidonic acid.

Answer

Cyclooxygenase-II (COX-II) is induced by cytokines at sites of inflammation.

Answer

Leukotrienes cause smooth muscle constriction.

Question 7

Which monoclonal antibody is used for Muckle-Wells syndrome?

Accepted Answer

Canakinumab

Answer

Catumaxomab

Answer

Ceolizumab

Answer

Cetuximab

Question 8

Etanercept is a biological disease-modifying agent used in the management of rheumatoid arthritis. What is its mechanism of action?

Accepted Answer

TNF alpha blockade

Answer

COX-2 inhibition

Answer

IL-6 inhibition

Answer

Stabilization of mast cells

Question 9

Allopurinol potentiates the action of which of the following drugs?

Accepted Answer

6-Mercaptopurine

Answer

Corticosteroids

Answer

Probenecid

Answer

Ampicillin

Question 10

The analgesic effect of Paracetamol is mediated by which receptor?

Accepted Answer

TRPV1

Answer

NK 1

Answer

BK1

Answer

Px23

Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs — MCQs

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