Analgesics and Anti-inflammatory Drugs Practice Questions

Q: Which monoclonal antibody is used for the treatment of Rheumatoid arthritis?

Anakinra. ### Explanation **Correct Option: A. Anakinra** Anakinra is a recombinant, non-glycosylated form of the human **Interleukin-1 (IL-1) receptor antagonist**. In Rheumatoid Arthritis (RA), IL-1 plays a key role in joint inflammation and cartilage degradation. By competitively inhibiting the binding of IL-1 to its receptor, Anakinra reduces the inflammatory response. While it is a biological DMARD (Disease-Modifying Antirheumatic Drug), it is technically a **receptor antagonist** rather than a traditional monoclonal antibody (which usually ends in *-mab*). However, in the context of this specific question, it is the designated biological agent for RA. **Analysis of Incorrect Options:** * **B. Leflunomide:** This is a **synthetic DMARD**. It works by inhibiting the enzyme **dihydroorotate dehydrogenase**, which interferes with pyrimidine synthesis, thereby inhibiting T-cell proliferation. It is not a monoclonal antibody. * **C. Adalimumab:** This is a monoclonal antibody against **TNF-α**. While it is used extensively in RA, it was not the designated answer in this specific set. (Note: In many clinical scenarios, Adalimumab is more commonly used than Anakinra). * **D. Sulfasalazine:** This is a **conventional synthetic DMARD**. It is a prodrug cleaved by colonic bacteria into sulfapyridine and 5-aminosalicylic acid (5-ASA). It is used for mild RA but is not a biological agent. **High-Yield Clinical Pearls for NEET-PG:** * **TNF-α Inhibitors:** Etanercept (decoy receptor), Infliximab (chimeric mAb), Adalimumab (human mAb). * **B-cell Depletion:** Rituximab (anti-CD20) is used in RA refractory to TNF inhibitors. * **T-cell Costimulation Blocker:** Abatacept (CTLA-4 Ig). * **IL-6 Receptor Antagonist:** Tocilizumab. * **JAK Inhibitors (Oral):** Tofacitinib and Baricitinib. * **Screening:** Always screen for **Latent Tuberculosis** before starting any biological DMARD (especially TNF inhibitors).

Q: Which newer monoclonal antibody is approved for rheumatoid arthritis?

Sarilumab. **Explanation:** **Correct Answer: D. Sarilumab** **Mechanism and Rationale:** Sarilumab is a human monoclonal antibody that acts as an **Interleukin-6 (IL-6) receptor antagonist**. IL-6 is a pro-inflammatory cytokine that plays a central role in the pathogenesis of Rheumatoid Arthritis (RA) by mediating joint inflammation and destruction. By binding to both soluble and membrane-bound IL-6 receptors, Sarilumab inhibits IL-6-mediated signaling. It is approved for patients with moderate-to-severe RA who have had an inadequate response or intolerance to one or more disease-modifying antirheumatic drugs (DMARDs), such as Methotrexate. **Analysis of Incorrect Options:** * **A, B, and C (Durvalumab, Pembrolizumab, Nivolumab):** These are all **Immune Checkpoint Inhibitors** used in Oncology. * **Pembrolizumab and Nivolumab** are PD-1 (Programmed Death-1) inhibitors. * **Durvalumab** is a PD-L1 inhibitor. * These drugs "release the brakes" on the immune system to treat cancers like melanoma and non-small cell lung cancer; they are not used for autoimmune conditions like RA. **High-Yield Clinical Pearls for NEET-PG:** * **IL-6 Inhibitors:** Apart from Sarilumab, **Tocilizumab** is the other major IL-6 receptor antagonist used in RA and Giant Cell Arteritis. * **TNF-α Inhibitors:** Remember the "Big 5"—Infliximab, Adalimumab, Etanercept, Certolizumab, and Golimumab. * **B-cell Depletion:** **Rituximab** (Anti-CD20) is used in RA if TNF inhibitors fail. * **T-cell Costimulation Blocker:** **Abatacept** (CTLA-4 Ig). * **JAK Inhibitors (Oral):** Tofacitinib and Baricitinib are non-monoclonal antibody targeted therapies for RA.

Q: All of the following are indications for eicosanoids or their inhibitors EXCEPT?

Essential hypertension. **Explanation:** The correct answer is **Essential Hypertension**. While eicosanoids (prostaglandins) have vasodilatory properties, they are not used in the clinical management of essential hypertension due to their short half-life, significant side effects, and the availability of more effective antihypertensive classes (e.g., ACE inhibitors, CCBs). In fact, NSAIDs (which inhibit prostaglandin synthesis) can actually worsen hypertension by causing sodium and water retention. **Analysis of Options:** * **Abortion:** Prostaglandin E1 (Misoprostol) and F2α (Carboprost) analogues are standard medical indications for inducing uterine contractions to terminate pregnancy or manage postpartum hemorrhage. * **Patent Ductus Arteriosus (PDA):** NSAIDs like **Indomethacin** or **Ibuprofen** (inhibitors of eicosanoid synthesis) are the treatment of choice to close a PDA in neonates by inhibiting the vasodilatory effect of PGE2. * **Transposition of the Great Arteries (TGA):** In cyanotic heart diseases where survival depends on a shunt, **Alprostadil (PGE1)** is administered to keep the ductus arteriosus open (maintain patency) until surgical intervention is possible. **High-Yield Clinical Pearls for NEET-PG:** * **PGE1 (Alprostadil):** Used for maintaining PDA in TGA and for erectile dysfunction. * **PGE1 Analogue (Misoprostol):** Used for NSAID-induced peptic ulcers and medical abortion. * **PGF2α (Latanoprost):** First-line treatment for Open-Angle Glaucoma (increases uveoscleral outflow). * **PGI2 (Epoprostenol):** Used in Pulmonary Arterial Hypertension. * **Aspirin:** The only irreversible COX inhibitor; used for cardioprotection at low doses.

Q: Which of the following drugs is used in severe hypertensive emergencies, is very short acting, and must be given by i.v. infusion?

Nitroprusside. **Explanation:** **Sodium Nitroprusside** is the drug of choice for hypertensive emergencies because it is a potent, balanced vasodilator (acting on both arterioles and venules). Its mechanism involves the release of nitric oxide (NO), which increases cGMP levels, leading to smooth muscle relaxation. The key features that make it the correct answer are: 1. **Rapid Onset:** It acts within seconds. 2. **Ultra-short Duration:** Its effect lasts only 1–5 minutes after stopping the infusion, allowing for precise "minute-to-minute" titration of blood pressure. 3. **Administration:** It is unstable in light and must be administered via continuous intravenous infusion using an infusion pump. **Analysis of Incorrect Options:** * **Diazoxide (A):** An arteriolar vasodilator formerly used for emergencies. However, it has a long half-life (24 hours) and can cause reflex tachycardia and hyperglycemia, making it less ideal than Nitroprusside. * **Hydralazine (B):** Primarily an arteriolar vasodilator. It is used in pregnancy-induced hypertension (Eclampsia) but has a slower onset and less predictable offset compared to Nitroprusside. * **Labetalol (C):** A combined alpha and beta-blocker. While used in hypertensive emergencies (especially aortic dissection), it can be given as an IV bolus and has a much longer duration of action (3–6 hours). **High-Yield Clinical Pearls for NEET-PG:** * **Cyanide Toxicity:** Nitroprusside metabolism releases cyanide. Toxicity is managed with **Sodium Thiosulfate** (donates sulfur) or **Hydroxocobalamin** (binds cyanide to form Cyanocobalamin). * **Light Sensitivity:** Nitroprusside solutions must be wrapped in aluminum foil to prevent photodegradation. * **Thiocyanate Toxicity:** Prolonged infusion can lead to thiocyanate accumulation, especially in patients with renal failure, causing psychosis and seizures.

Q: Which of the following statements about NSAIDs is false?

NSAIDs are useful in neuropathic pain.. **Explanation:** **Why Option C is the correct (False) statement:** NSAIDs primarily work by inhibiting the enzyme Cyclooxygenase (COX), thereby reducing the synthesis of prostaglandins which mediate peripheral inflammation and nociception. **Neuropathic pain**, however, is caused by a lesion or disease of the somatosensory nervous system (e.g., Diabetic Neuropathy, Post-herpetic neuralgia). It does not respond well to conventional analgesics like NSAIDs or Opioids. The first-line treatments for neuropathic pain are **Gabapentinoids** (Gabapentin, Pregabalin), **TCAs** (Amitriptyline), or **SNRIs** (Duloxetine). **Analysis of other options:** * **Option A (True):** NSAIDs inhibit the synthesis of vasodilatory prostaglandins (PGE2 and PGI2) in the kidneys. This leads to sodium and water retention and blunts the pressure-natriuresis response, thereby interfering with the efficacy of diuretics and ACE inhibitors. * **Option B (True):** Prostaglandins maintain renal perfusion by dilating the afferent arteriole. By inhibiting these, NSAIDs cause vasoconstriction, which can lead to **Acute Kidney Injury (AKI)**, especially in patients with pre-existing renal disease, CCF, or dehydration. * **Option D (True):** Several NSAIDs like Diclofenac, Ketoprofen, and Ibuprofen are available as topical gels or patches. These provide localized pain relief with significantly lower systemic absorption and fewer GI side effects. **High-Yield Clinical Pearls for NEET-PG:** * **Triple Whammy:** The dangerous combination of an **NSAID + ACE Inhibitor + Diuretic** which significantly increases the risk of AKI. * **Aspirin:** The only NSAID that irreversibly inhibits COX-1 (via acetylation). * **Analgesic Nephropathy:** Chronic use of NSAID combinations can lead to **Renal Papillary Necrosis** and chronic interstitial nephritis.

Q: What is the mechanism of action of aspirin?

Inhibits COX 1 and COX 2 irreversibly. ### Explanation **Correct Option: D (Inhibits COX 1 and COX 2 irreversibly)** Aspirin (Acetylsalicylic acid) is unique among Non-Steroidal Anti-inflammatory Drugs (NSAIDs). It works by **covalently acetylating** a serine residue at the active site of the Cyclooxygenase (COX) enzyme. This chemical modification results in the **irreversible inhibition** of both COX-1 and COX-2 isoforms. Because the inhibition is irreversible, the enzyme is permanently inactivated; the cell must synthesize new enzyme molecules to restore activity. **Analysis of Incorrect Options:** * **Option A & B:** While aspirin is more potent against COX-1 (especially at low doses), it is not a "preferential" inhibitor in the pharmacological sense used for drugs like Meloxicam or Etodolac. It acts on both isoforms. * **Option C:** Most other NSAIDs (like Ibuprofen or Naproxen) bind to the enzyme via non-covalent, competitive bonds, making their action **reversible**. Aspirin is the classic exception to this rule. **NEET-PG High-Yield Pearls:** 1. **Antiplatelet Effect:** Platelets lack a nucleus and cannot synthesize new COX-1. Therefore, a single low dose of aspirin inhibits thromboxane $A_2$ ($TXA_2$) production for the entire lifespan of the platelet (approx. 8–11 days). 2. **Zero-Order Kinetics:** At high/toxic doses (salicylism), aspirin metabolism shifts from first-order to zero-order kinetics. 3. **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. 4. **Aspirin Triad (Samter’s Triad):** Asthma, nasal polyposis, and aspirin hypersensitivity.

Q: Anakinra, used in the treatment of rheumatoid arthritis, is which of the following biological agents?

Interleukin-1 (IL-1). **Explanation:** **Anakinra** is a recombinant, non-glycosylated form of the human **Interleukin-1 receptor antagonist (IL-1Ra)**. In the pathogenesis of Rheumatoid Arthritis (RA), IL-1 is a key pro-inflammatory cytokine that mediates cartilage degradation and bone resorption. Anakinra works by competitively inhibiting the binding of IL-1 (both IL-1α and IL-1β) to its type I receptor, thereby neutralizing its inflammatory effects. **Analysis of Options:** * **Option A (Correct):** Anakinra is specifically designed to target the **IL-1** pathway. It is used in RA patients who have failed one or more Disease-Modifying Antirheumatic Drugs (DMARDs). * **Option B & C (Incorrect):** Drugs targeting **TNF-alpha** include Etanercept (decoy receptor), Infliximab, and Adalimumab (monoclonal antibodies). TNF-beta (Lymphotoxin-alpha) is not the primary target of these common biological DMARDs. * **Option D (Incorrect):** **IL-7** is involved in T-cell homeostasis but is not a target for currently approved biological therapies in the management of Rheumatoid Arthritis. **High-Yield Clinical Pearls for NEET-PG:** * **Canakinumab:** A human monoclonal antibody against **IL-1β** (used in Gout and Periodic Fever Syndromes). * **Rilonacept:** An **IL-1 trap** (ligand-binding domain of IL-1 receptor) used in Cryopyrin-Associated Periodic Syndromes (CAPS). * **Key Side Effect:** Injection site reactions are common. Importantly, Anakinra should **never** be combined with TNF-inhibitors due to a significantly increased risk of serious infections. * **Other Biologicals:** Tocilizumab (IL-6 inhibitor), Abatacept (CTLA-4 analog/T-cell costimulation blocker), and Rituximab (Anti-CD20).

Question 1

Which monoclonal antibody is used for the treatment of Rheumatoid arthritis?

Accepted Answer

Anakinra

Answer

Leflunomide

Answer

Adalimumab

Answer

Sulfasalazine

Question 2

Which of the following statements is true of ketorolac?

Accepted Answer

Its analgesic efficacy is equal to morphine in postoperative pain

Answer

Has potent anti-inflammatory activity

Answer

Is used as preanesthetic analgesic

Answer

It interacts with opioid receptors

Question 3

Which newer monoclonal antibody is approved for rheumatoid arthritis?

Accepted Answer

Sarilumab

Answer

Durvalumab

Answer

Pembrolizumab

Answer

Nivolumab

Question 4

All of the following are indications for eicosanoids or their inhibitors EXCEPT?

Accepted Answer

Essential hypertension

Answer

Abortion

Answer

Patent ductus arteriosus

Answer

Transposition of the great arteries

Question 5

Which of the following drugs is used in severe hypertensive emergencies, is very short acting, and must be given by i.v. infusion?

Accepted Answer

Nitroprusside

Answer

Diazoxide

Answer

Hydralazine

Answer

Labetalol

Question 6

Which of the following statements about NSAIDs is false?

Accepted Answer

NSAIDs are useful in neuropathic pain.

Answer

They interfere with the antihypertensive effect of diuretics.

Answer

NSAIDs should be avoided in renal disease as they can cause nephrotoxicity.

Answer

Many NSAIDs can be used topically.

Question 7

What is the mechanism of action of aspirin?

Accepted Answer

Inhibits COX 1 and COX 2 irreversibly

Answer

Inhibits COX-2 preferentially

Answer

Inhibits COX-1 preferentially

Answer

Inhibits COX 1 and COX 2 reversibly

Question 8

Anakinra, used in the treatment of rheumatoid arthritis, is which of the following biological agents?

Accepted Answer

Interleukin-1 (IL-1)

Answer

Tumor Necrosis Factor alpha (TNF-alpha)

Answer

Tumor Necrosis Factor beta (TNF-beta)

Answer

Interleukin-7 (IL-7)

Question 9

All of the following actions of aspirin are mediated by inhibition of prostaglandin synthesis EXCEPT:

Accepted Answer

Hyperventilation

Answer

Analgesia

Answer

Closure of patent ductus arteriosus

Answer

Bleeding tendency

Question 10

Which of the following shows regressive metamorphosis?

Accepted Answer

Hydatid cyst

Answer

Cysticercoid

Answer

Cysticercus bovis

Answer

Cysticercus cellulosae

Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs — MCQs

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