Analgesics and Anti-inflammatory Drugs — MCQs

A 30-year-old male presents with sudden onset pain, swelling, and redness of the left first metatarsophalangeal joint. A needle aspirate of the joint shows needle-shaped, negatively birefringent crystals. The patient was prescribed a medication and returned the next day with nausea, vomiting, and diarrhea after taking it. Which of the following is the most likely medication that was prescribed?

Q138Easy

All drugs are used in the management of psoriatic arthritis except?

Q139Easy

What is the loading dose of leflunomide in rheumatoid arthritis?

Q140Easy

Which of the following is/are cyclo-oxygenase inhibitors?

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

Question 131: In low doses, aspirin inhibits which of the following enzymes?

A. Lipoxygenase
B. Cyclo-oxygenase (Correct Answer)
C. Thromboxane A2
D. Prostaglandin I2

Explanation: **Explanation:** Aspirin (Acetylsalicylic acid) is a non-steroidal anti-inflammatory drug (NSAID) that works by **irreversibly inhibiting the Cyclo-oxygenase (COX)** enzyme. It achieves this by acetylating a serine residue at the active site of the enzyme, thereby blocking the synthesis of prostaglandins and thromboxanes. **Why Option B is Correct:** Aspirin is unique among NSAIDs because of its irreversible action. In **low doses (75–150 mg/day)**, aspirin selectively inhibits **COX-1** in platelets. Since platelets are anucleated and cannot synthesize new enzymes, the inhibition lasts for the entire lifespan of the platelet (approx. 8–11 days), leading to its potent anti-platelet effect. **Why Other Options are Incorrect:** * **A. Lipoxygenase:** Aspirin does not inhibit the lipoxygenase (LOX) pathway. In fact, by blocking the COX pathway, arachidonic acid may be shunted toward the LOX pathway, potentially increasing leukotriene production (the mechanism behind aspirin-induced asthma). * **C & D. Thromboxane A2 and Prostaglandin I2:** These are **products** of the COX pathway, not enzymes themselves. While aspirin reduces the levels of TXA2 and PGI2, the question specifically asks for the *enzyme* being inhibited. **High-Yield Clinical Pearls for NEET-PG:** * **Zero-order kinetics:** Aspirin follows first-order kinetics at low doses but shifts to zero-order kinetics at high/toxic doses. * **Reye’s Syndrome:** Aspirin is contraindicated in children with viral infections (except in Kawasaki disease) due to the risk of hepatic encephalopathy. * **Aspirin Triad (Samter’s Triad):** Asthma, nasal polyposis, and aspirin hypersensitivity. * **Antidote for Salicylate poisoning:** Sodium bicarbonate (to alkalinize urine and promote excretion).

Question 132: What is the drug of choice for relieving pain in myocardial infarction?

A. Morphine (Correct Answer)
B. Fortwin
C. Diazepam
D. NSAID

Explanation: **Explanation:** **Morphine** is the drug of choice for managing the intense chest pain associated with acute myocardial infarction (MI) [2]. Its efficacy is due to a dual mechanism: 1. **Analgesia:** It is a potent opioid agonist that provides rapid relief from severe pain [2]. 2. **Hemodynamic Benefits:** Morphine acts as a **venodilator**, reducing venous return (preload) and decreasing the workload on the heart [3]. It also reduces sympathetic overactivity, which lowers myocardial oxygen demand and alleviates the patient's anxiety/apprehension. **Analysis of Incorrect Options:** * **B. Fortwin (Pentazocine):** This is a partial opioid agonist/antagonist. It is avoided in MI because it can increase systemic and pulmonary arterial pressure and heart rate, thereby **increasing myocardial oxygen demand**, which can worsen the infarct. * **C. Diazepam:** While it is a benzodiazepine used to reduce anxiety, it has no analgesic properties and cannot manage the severe pain of an MI. * **D. NSAIDs:** These are generally **contraindicated** in the acute phase of MI (except for Aspirin). NSAIDs can increase the risk of myocardial rupture, impair infarct healing, and increase the risk of re-infarction and heart failure. **High-Yield Clinical Pearls for NEET-PG:** * **M.O.N.A. Protocol:** The classic mnemonic for initial MI management is **M**orphine, **O**xygen, **N**itroglycerin, and **A**spirin [1]. * **Route:** Morphine should be administered **Intravenously (IV)**. Intramuscular (IM) injections are avoided as they can cause erratic absorption and interfere with CK-MB enzyme levels used for diagnosis. * **Antidote:** In case of morphine-induced respiratory depression, **Naloxone** is the specific antagonist. * **Caution:** Morphine should be used cautiously in **Right Ventricular MI** or inferior wall MI due to the risk of severe hypotension.

Question 133: A common side effect associated with all NSAID drugs is?

A. Drowsiness
B. Gastric irritation (Correct Answer)
C. Xerostomia
D. Constipation

Explanation: **Explanation:** The primary mechanism of action for Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) is the inhibition of the enzyme **Cyclooxygenase (COX)**. This prevents the conversion of arachidonic acid into prostaglandins (PGs). **Gastric irritation** is the most common side effect because NSAIDs inhibit **COX-1**, which is responsible for synthesizing "housekeeping" prostaglandins (**PGE2 and PGI2**) in the gastric mucosa. These prostaglandins are cytoprotective; they increase bicarbonate secretion, enhance mucosal blood flow, and promote mucus production. By inhibiting their synthesis, NSAIDs increase gastric acid secretion and weaken the mucosal barrier, leading to dyspepsia, erosions, and peptic ulcers. **Analysis of Incorrect Options:** * **Drowsiness:** This is not a characteristic side effect of NSAIDs. It is more commonly associated with opioid analgesics or first-generation antihistamines. * **Xerostomia (Dry mouth):** This is a classic anticholinergic side effect (e.g., Atropine, TCAs) and is not typically caused by NSAIDs. * **Constipation:** This is the most common gastrointestinal side effect of **Opioids** (due to decreased intestinal motility). In contrast, some NSAIDs (like Mefenamic acid) may actually cause diarrhea. **High-Yield Clinical Pearls for NEET-PG:** * **Selective COX-2 Inhibitors (e.g., Celecoxib):** Developed to reduce gastric irritation, but carry a higher risk of cardiovascular thrombotic events. * **Misoprostol:** A PGE1 analogue used to prevent NSAID-induced gastric ulcers. * **Aspirin Sensitivity:** Inhibition of COX can shift arachidonic acid metabolism toward the lipoxygenase (LOX) pathway, increasing leukotrienes and potentially triggering **aspirin-exacerbated respiratory disease (AERD)** or "Aspirin Asthma."

Question 134: What is the mechanism of action of allopurinol?

A. Inhibits the synthesis of uric acid (Correct Answer)
B. Inhibits the tubular reabsorption of uric acid
C. Anti-inflammatory action
D. Increases phagocytosis of urate crystals

Explanation: ### Explanation **Correct Answer: A. Inhibits the synthesis of uric acid** **Mechanism of Action:** Allopurinol is a hypouricemic agent that acts as a **competitive inhibitor of Xanthine Oxidase**, the enzyme responsible for converting hypoxanthine to xanthine and xanthine to uric acid [1], [2]. Allopurinol is a structural analog (isomer) of hypoxanthine [1]. It is metabolized by xanthine oxidase into its active metabolite, **Alloxanthine (Oxypurinol)**, which is a non-competitive, long-acting inhibitor of the same enzyme [1], [2]. By blocking this pathway, allopurinol effectively reduces the plasma concentration and urinary excretion of uric acid, making it the drug of choice for chronic gout [2]. **Analysis of Incorrect Options:** * **B. Inhibits tubular reabsorption:** This describes **Uricosuric drugs** like Probenecid and Sulfinpyrazone [1]. These drugs act on the URAT-1 transporter in the proximal tubule to increase uric acid excretion. * **C. Anti-inflammatory action:** This is the mechanism of **NSAIDs** (e.g., Naproxen, Indomethacin) and **Corticosteroids**, which are used to manage pain and inflammation during acute gouty attacks. Allopurinol has no inherent anti-inflammatory properties. * **D. Increases phagocytosis:** This is incorrect. **Colchicine**, used in acute gout, actually *inhibits* the migration of granulocytes and reduces the phagocytosis of urate crystals by binding to tubulin. **High-Yield Clinical Pearls for NEET-PG:** * **Acute Attack Risk:** Allopurinol should **never** be started during an acute attack of gout, as a sudden drop in serum urate can mobilize crystals from tissues and worsen the inflammation [1]. * **Drug Interaction:** It significantly increases the toxicity of **6-Mercaptopurine (6-MP)** and **Azathioprine** because these drugs are metabolized by xanthine oxidase. * **Adverse Effects:** The most serious side effect is **Stevens-Johnson Syndrome (SJS)**, particularly in patients with the **HLA-B*5801** allele.

Question 135: Gum hypertrophy is an adverse effect of which of the following drugs when used at therapeutic levels?

A. Phenobarbitone
B. Phenytoin (Correct Answer)
C. Carbamazepine
D. Sodium valproate

Explanation: **Explanation:** **Phenytoin** is a classic cause of **Gingival Hyperplasia (Gum Hypertrophy)**, occurring in approximately 30–50% of patients. The underlying mechanism involves the drug’s effect on calcium metabolism and the stimulation of **platelet-derived growth factor (PDGF)**. This leads to the over-proliferation of gingival fibroblasts and increased collagen synthesis. Poor oral hygiene is a significant risk factor, and the condition often regresses upon drug discontinuation. **Analysis of Incorrect Options:** * **Phenobarbitone:** Primarily causes sedation, cognitive impairment, and skin rashes. It does not typically affect the gums. * **Carbamazepine:** Common side effects include diplopia, ataxia, and hyponatremia (SIADH). It is notably "gingival-neutral." * **Sodium Valproate:** Known for causing weight gain, alopecia (curly hair regrowth), hepatotoxicity, and pancreatitis. While it can cause transient thrombocytopenia, it does not cause gum hypertrophy. **High-Yield Clinical Pearls for NEET-PG:** * **Other Drugs causing Gingival Hyperplasia:** Remember the mnemonic **"PNC"** — **P**henytoin, **N**ifedipine (and other Calcium Channel Blockers like Verapamil/Amlodipine), and **C**yclosporine. * **Phenytoin Side Effects Mnemonic (HOT MALAYALAM):** **H**irsutism, **O**steomalacia, **T**eratogenicity (Fetal Hydantoin Syndrome), **M**egaloblastic anemia, **A**taxia, **L**ymphadenopathy, **A**rrhythmias, **Y**ellow-brown skin, **A**denopathy, **L**eukopenia, **A**nd **M**outh (Gingival Hyperplasia). * **Zero-Order Kinetics:** Phenytoin follows capacity-limited elimination at therapeutic/high doses, making its plasma concentration unpredictable.

Question 136: Methotrexate is used for the management of all of the following conditions except?

A. Rheumatoid arthritis
B. Psoriasis
C. Sickle cell anemia (Correct Answer)
D. Organ transplantation

Explanation: **Explanation:** **1. Why Sickle Cell Anemia is the Correct Answer:** Methotrexate (MTX) is a folate antagonist that inhibits the enzyme **dihydrofolate reductase (DHFR)**, leading to a decrease in DNA synthesis and cell proliferation [1]. It has no role in the management of Sickle Cell Anemia. The drug of choice for reducing the frequency of painful crises in Sickle Cell Anemia is **Hydroxyurea** [3], which acts by increasing the levels of Fetal Hemoglobin (HbF) [3]. **2. Analysis of Incorrect Options:** * **Rheumatoid Arthritis (RA):** MTX is the **"Anchor Drug"** and the first-line Disease-Modifying Anti-Rheumatic Drug (DMARD) for RA [2]. It acts by increasing adenosine levels, which exerts a potent anti-inflammatory effect. * **Psoriasis:** MTX is highly effective for severe, recalcitrant psoriasis and psoriatic arthritis due to its ability to inhibit the rapid proliferation of epidermal keratinocytes [2]. * **Organ Transplantation:** In low doses, MTX acts as an immunosuppressant used to prevent Graft-versus-Host Disease (GVHD) and organ rejection by inhibiting T-cell activation and proliferation [2]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Competitive inhibition of DHFR; cell cycle-specific for the **S-phase** [1]. * **Toxicity:** Bone marrow suppression (most common), hepatotoxicity (cirrhosis), and pulmonary fibrosis [4]. * **Rescue Therapy:** **Leucovorin (Folinic acid)** is used to "rescue" normal cells from MTX toxicity by bypassing the inhibited DHFR enzyme [1], [4]. * **Contraindication:** It is highly **teratogenic** (causes neural tube defects and fetal death) [4]. * **Other Uses:** Choriocarcinoma (Drug of choice), Ectopic pregnancy, and Osteosarcoma.

Question 137: A 30-year-old male presents with sudden onset pain, swelling, and redness of the left first metatarsophalangeal joint. A needle aspirate of the joint shows needle-shaped, negatively birefringent crystals. The patient was prescribed a medication and returned the next day with nausea, vomiting, and diarrhea after taking it. Which of the following is the most likely medication that was prescribed?

A. Allopurinol
B. Colchicine (Correct Answer)
C. Steroids
D. Indomethacin

Explanation: ### Explanation **Diagnosis:** The clinical presentation of sudden onset pain, swelling, and redness of the first metatarsophalangeal joint (podagra), combined with the presence of **needle-shaped, negatively birefringent crystals**, is diagnostic of **Acute Gouty Arthritis**. **1. Why Colchicine is the Correct Answer:** Colchicine is a first-line agent for acute gout. Its mechanism involves binding to tubulin, inhibiting microtubule polymerization, which prevents leukocyte migration and phagocytosis. However, it has a very narrow therapeutic index. Its most common and characteristic adverse effects are **gastrointestinal (GI) toxicity**, specifically nausea, vomiting, and **profuse diarrhea**. These symptoms occur because colchicine inhibits the rapid turnover of GI mucosal cells. **2. Why the Other Options are Incorrect:** * **A. Allopurinol:** This is a Xanthine Oxidase inhibitor used for *chronic* management (urates-lowering therapy). It is **contraindicated** during an acute attack as it can worsen inflammation by causing rapid fluctuations in serum urate levels. It does not typically cause acute diarrhea. * **C. Steroids:** Glucocorticoids are used in acute gout (especially if NSAIDs/Colchicine are contraindicated), but their side effects include hyperglycemia and hypertension, not immediate acute diarrhea. * **D. Indomethacin:** This is a potent NSAID often used as a first-line treatment for gout. While it can cause GI upset or peptic ulcers, the classic "diarrhea" side effect described in the clinical vignette is much more characteristic of Colchicine toxicity. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Colchicine:** Inhibits microtubule assembly by binding to tubulin. * **Dose-limiting toxicity:** Diarrhea is the earliest sign of toxicity. * **Chronic toxicity:** Can lead to agranulocytosis, aplastic anemia, and myopathy. * **Acute Gout Management:** NSAIDs (e.g., Indomethacin, Naproxen) are generally preferred over Colchicine due to the latter's toxicity profile. * **Crystal Morphology:** Gout = Needle-shaped, negatively birefringent (Yellow when parallel to the axis); Pseudogout = Rhomboid-shaped, positively birefringent (Blue).

Question 138: All drugs are used in the management of psoriatic arthritis except?

A. Methotrexate
B. Leflunomide
C. Chloroquine (Correct Answer)
D. Abatacept

Explanation: **Explanation:** The correct answer is **Chloroquine**. **Why Chloroquine is the correct answer:** Chloroquine and Hydroxychloroquine are Antimalarial drugs commonly used as DMARDs (Disease-Modifying Antirheumatic Drugs) for Rheumatoid Arthritis and SLE. However, they are **contraindicated or avoided in Psoriatic Arthritis** because they can trigger or significantly exacerbate skin lesions, leading to severe exfoliative dermatitis or "psoriasis flare-ups." Therefore, they are not used in the management of this condition. **Analysis of other options:** * **A. Methotrexate:** This is the first-line conventional synthetic DMARD for psoriatic arthritis. It effectively treats both the joint inflammation and the underlying skin psoriasis. * **B. Leflunomide:** An alternative conventional DMARD used in patients who cannot tolerate methotrexate. It inhibits dihydroorotate dehydrogenase and is effective for peripheral joint involvement in psoriatic arthritis. * **D. Abatacept:** A biological DMARD that acts as a T-cell costimulation modulator (CTLA-4 Ig). It is FDA-approved for the treatment of active psoriatic arthritis in adults. **Clinical Pearls for NEET-PG:** * **First-line treatment:** NSAIDs for mild cases; Methotrexate for moderate-to-severe disease. * **TNF-inhibitors:** (e.g., Etanercept, Adalimumab) are highly effective for both skin and joint symptoms. * **IL-17 Inhibitors:** (e.g., Secukinumab) are specifically high-yield for psoriatic arthritis management. * **Avoid:** Systemic corticosteroids are generally avoided in psoriasis due to the risk of life-threatening **pustular psoriasis** upon withdrawal.

Question 139: What is the loading dose of leflunomide in rheumatoid arthritis?

A. 20 mg
B. 10 mg
C. 100 mg (Correct Answer)
D. 400 mg

Explanation: **Explanation:** **Leflunomide** is a Disease-Modifying Antirheumatic Drug (DMARD) that acts by inhibiting the enzyme **dihydroorotate dehydrogenase (DHODH)**. This inhibition leads to the depletion of intracellular pyrimidine pools, thereby arresting the proliferation of activated T-cells. **Why 100 mg is correct:** Leflunomide has a very long half-life (approximately **2 weeks**) due to extensive enterohepatic circulation. To achieve therapeutic steady-state plasma concentrations rapidly, a **loading dose of 100 mg once daily for 3 consecutive days** is administered. Without this loading dose, it would take several weeks to reach effective levels. **Analysis of incorrect options:** * **10 mg & 20 mg:** These represent the standard **maintenance doses**. After the initial 3-day loading period, patients are typically transitioned to 20 mg daily (or 10 mg if the higher dose is not tolerated). * **400 mg:** This is an excessively high dose and is not used in standard rheumatological practice; it would significantly increase the risk of hepatotoxicity and gastrointestinal distress. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Pyrimidine synthesis inhibitor (DHODH inhibitor). * **Active Metabolite:** Malononitrilamide (MNA) / A77 1726. * **Washout Procedure:** Due to its long half-life, if a patient experiences toxicity or wishes to become pregnant, **Cholestyramine** is used to interrupt enterohepatic circulation and accelerate drug elimination. * **Contraindication:** It is highly **teratogenic** (Category X) and contraindicated in pregnancy. * **Monitoring:** Baseline and periodic Liver Function Tests (LFTs) are mandatory due to the risk of hepatotoxicity.

Question 140: Which of the following is/are cyclo-oxygenase inhibitors?

A. Aspirin
B. Indomethacin
C. Rofecoxib
D. All of these (Correct Answer)

Explanation: **Explanation:** The correct answer is **D (All of these)**. The underlying medical concept involves the mechanism of action of Non-Steroidal Anti-inflammatory Drugs (NSAIDs), which exert their effects by inhibiting the enzyme **Cyclo-oxygenase (COX)**. This enzyme is responsible for converting arachidonic acid into prostaglandins, prostacyclin, and thromboxane. * **Aspirin:** It is a non-selective COX inhibitor. Its unique feature is that it **irreversibly** acetylates the COX enzyme, leading to long-lasting anti-platelet effects. * **Indomethacin:** It is a potent, non-selective, reversible COX inhibitor. It is a traditional NSAID often used for acute gout and patent ductus arteriosus (PDA). * **Rofecoxib:** It belongs to the "coxib" class, which are **selective COX-2 inhibitors**. While it specifically targets the inducible COX-2 isoform (sparing the constitutive COX-1), it is still fundamentally a cyclo-oxygenase inhibitor. **High-Yield Clinical Pearls for NEET-PG:** * **COX-1 vs. COX-2:** COX-1 is "constitutive" (housekeeping functions like gastric protection), while COX-2 is "inducible" (expressed during inflammation). * **Aspirin Overdose:** Follows zero-order kinetics and can lead to Salicylism (tinnitus, respiratory alkalosis followed by metabolic acidosis). * **Selective COX-2 Inhibitors:** They have a lower risk of gastric ulcers but carry an increased risk of **cardiovascular thrombotic events** (due to the inhibition of PGI2 without affecting TXA2). * **Drug of Choice:** Indomethacin is the classic drug of choice for closing a **Patent Ductus Arteriosus (PDA)** in neonates.

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