Analgesics and Anti-inflammatory Drugs Practice Questions

Q: Which of the following is responsible for housekeeping functions?

COX1. ### Explanation The correct answer is **COX1 (Cyclooxygenase-1)**. #### 1. Why COX1 is the Correct Answer Cyclooxygenase-1 (COX1) is known as a **constitutive enzyme**, meaning it is expressed at constant levels in most tissues under normal physiological conditions. It is responsible for "housekeeping" functions because it produces prostaglandins (PGs) that maintain vital organ homeostasis. These functions include: * **Gastric Protection:** Synthesis of PGE2 and PGI2, which inhibit acid secretion and promote protective mucus/bicarbonate production. * **Renal Homeostasis:** Maintaining renal blood flow and glomerular filtration rate (GFR). * **Platelet Aggregation:** Production of Thromboxane A2 (TXA2) for normal clotting. #### 2. Why Other Options are Incorrect * **COX2:** This is primarily an **inducible enzyme**. Its expression is triggered by inflammatory stimuli (cytokines, growth factors, endotoxins) at the site of injury. While it has some constitutive roles (in the brain, kidney, and bone), its main role is mediating pain, fever, and inflammation. * **COX3:** This is a variant of COX1 (often called COX-1b) found predominantly in the cerebral cortex. It is thought to be the primary target for Paracetamol, but it does not perform systemic housekeeping functions. #### 3. High-Yield Clinical Pearls for NEET-PG * **Aspirin:** Irreversibly inhibits COX1 (at low doses) and COX2. * **Selective COX2 Inhibitors (e.g., Celecoxib):** These spare the "housekeeping" COX1, reducing the risk of gastric ulcers, but carry a higher risk of **thrombotic cardiovascular events** because they inhibit PGI2 (vasodilator) without affecting TXA2 (vasoconstrictor). * **Glucocorticoids:** These act by inhibiting the expression of the COX2 gene. * **The "Housekeeping" Mnemonic:** **COX1** is for **1** (One) body to maintain; **COX2** is for **2** (Too) much inflammation.

Q: Allopurinol is used in the treatment of which of the following conditions?

Gout. **Explanation:** **Correct Answer: B. Gout** Allopurinol is the drug of choice for the long-term management of **chronic gout**. It is a **Hypoxanthine analog** that acts as a potent **Xanthine Oxidase inhibitor**. By inhibiting this enzyme, it prevents the conversion of hypoxanthine to xanthine and xanthine to uric acid, thereby reducing serum urate levels (Hypouricemic agent). This prevents the deposition of monosodium urate crystals in joints and kidneys. **Why other options are incorrect:** * **A. Osteoarthritis:** This is a degenerative joint disease characterized by cartilage wear and tear. Treatment focuses on lifestyle modification, physical therapy, and analgesics like NSAIDs or intra-articular steroids, not urate-lowering therapy. * **C. Rheumatoid Arthritis (RA):** RA is an autoimmune inflammatory disorder. Management requires Disease-Modifying Anti-Rheumatic Drugs (DMARDs) like Methotrexate, Sulfasalazine, or biologicals (TNF-inhibitors) to suppress the immune response. * **D. Ankylosing Spondylitis:** This is a seronegative spondyloarthropathy primarily affecting the spine. Treatment involves NSAIDs, exercise, and TNF-alpha inhibitors. **NEET-PG High-Yield Pearls:** * **Acute Gout Warning:** Never start Allopurinol during an acute attack of gout, as a sudden change in urate levels can precipitate or worsen the flare. * **Drug Interactions:** Allopurinol inhibits the metabolism of **6-Mercaptopurine** and **Azathioprine**. If co-administered, the dose of these drugs must be reduced by 75% to avoid life-threatening bone marrow suppression. * **Adverse Effects:** The most serious side effect is **Allopurinol Hypersensitivity Syndrome** (including Stevens-Johnson Syndrome), which is strongly associated with the **HLA-B*5801** allele. * **Alternative:** **Febuxostat** is a non-purine selective inhibitor of xanthine oxidase used in patients intolerant to Allopurinol.

Q: Which of the following is NOT a TNF–α antagonist used in rheumatoid arthritis?

Ifosfamide. ### Explanation The correct answer is **Ifosfamide**. **1. Why Ifosfamide is the correct answer:** Ifosfamide is an **alkylating agent** belonging to the nitrogen mustard group. It is a cytotoxic chemotherapy drug used primarily in the treatment of various cancers (e.g., testicular cancer, sarcomas, lymphomas) [2]. It works by cross-linking DNA strands, thereby inhibiting DNA replication. It has no role as a TNF-α antagonist and is not used in the management of rheumatoid arthritis (RA). **2. Analysis of Incorrect Options (TNF-α Antagonists):** TNF-α (Tumor Necrosis Factor-alpha) is a key pro-inflammatory cytokine involved in the pathogenesis of RA. The following are Biological Disease-Modifying Antirheumatic Drugs (bDMARDs) that target it: * **Infliximab:** A chimeric monoclonal antibody that binds to both soluble and transmembrane TNF-α. * **Etanercept:** A soluble **fusion protein** (TNF receptor linked to the Fc fraction of IgG1) that acts as a "decoy receptor" to soak up circulating TNF-α [1]. * **Adalimumab:** A fully human recombinant monoclonal antibody against TNF-α. **3. High-Yield Clinical Pearls for NEET-PG:** * **Ifosfamide Toxicity:** A high-yield side effect is **Hemorrhagic Cystitis**, caused by the metabolite **Acrolein**. This is prevented by aggressive hydration and the administration of **MESNA** (2-Mercaptoethane sulfonate Na). * **TNF-α Inhibitor Screening:** Before starting any TNF-α antagonist, patients **must** be screened for **Latent Tuberculosis** (using TST or IGRA) because these drugs can cause reactivation of TB. * **Other TNF-α Inhibitors:** Certolizumab (pegylated) and Golimumab [1]. * **Memory Aid:** Remember the "mabs" (monoclonal antibodies) and the "cept" (receptor) for TNF blockers. Ifosafamide sounds like Cyclophosphamide, both of which are anticancer alkylators.

Q: Which of the following enzymes is inhibited by Aspirin?

Cyclooxygenase. **Explanation:** **1. Why Cyclooxygenase (COX) is the correct answer:** Aspirin (Acetylsalicylic acid) belongs to the Non-Steroidal Anti-Inflammatory Drug (NSAID) class. Its primary mechanism of action is the **irreversible inhibition** of 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 blockade prevents the conversion of arachidonic acid into Prostaglandins (mediators of pain and inflammation) and Thromboxane A2 (a potent platelet aggregator). **2. Why the other options are incorrect:** * **Lipooxygenase (LOX):** This enzyme converts arachidonic acid into Leukotrienes. Aspirin does not inhibit LOX; in fact, by blocking the COX pathway, Aspirin can "shunt" arachidonic acid toward the LOX pathway, potentially leading to Aspirin-Exacerbated Respiratory Disease (AERD) or "Aspirin Asthma." * **Phospholipase:** Specifically Phospholipase A2, this enzyme releases arachidonic acid from membrane phospholipids. It is inhibited by **Corticosteroids** (via lipocortin/annexin A1), not by NSAIDs like Aspirin. **3. High-Yield Clinical Pearls for NEET-PG:** * **Irreversibility:** Aspirin is the only NSAID that inhibits COX irreversibly. Because platelets cannot synthesize new enzymes, the antiplatelet effect lasts for the life 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 (like Varicella or Influenza) due to the risk of fulminant hepatic failure and encephalopathy. * **Therapeutic Doses:** Low dose (<325 mg) is used for antiplatelet effects; higher doses are required for analgesic and anti-inflammatory actions.

Q: Which of the following is NOT a side effect of paroxetine?

Premature ejaculation. Paroxetine is a Selective Serotonin Reuptake Inhibitor (SSRI). The core concept to understand here is that **SSRIs are notorious for causing sexual dysfunction** [1, 2], but they specifically **delay ejaculation** rather than causing it prematurely [2]. **Why Option A is the Correct Answer:** Paroxetine increases serotonin levels in the synaptic cleft. Serotonin has an inhibitory effect on ejaculation. Therefore, paroxetine causes **delayed ejaculation** (ejaculatory retardation) [2]. Because of this "side effect," paroxetine and other SSRIs (like Dapoxetine) are actually used therapeutically to treat premature ejaculation [4]. Thus, premature ejaculation is not a side effect; it is the condition the drug treats. **Analysis of Incorrect Options:** * **B & C (Erectile Dysfunction & Decreased Libido):** These are very common side effects of SSRIs. Increased serotonin stimulation of 5-HT2 receptors in the CNS leads to decreased sexual desire (libido) and difficulty maintaining an erection [2]. * **D (Diarrhea):** Approximately 90% of the body's serotonin is in the GI tract. SSRIs increase serotonergic activity in the gut, leading to increased motility, which commonly manifests as nausea, vomiting, or diarrhea [2]. **NEET-PG High-Yield Pearls:** * **Dapoxetine:** The specific SSRI approved for the "on-demand" treatment of premature ejaculation due to its rapid onset and short half-life. * **Most Sedating SSRI:** Paroxetine (also has significant anticholinergic properties). * **Discontinuation Syndrome:** Paroxetine has a short half-life, making it the SSRI most likely to cause withdrawal symptoms if stopped abruptly [3]. * **Drug of Choice for Sexual Dysfunction:** If a patient develops sexual side effects on SSRIs, switching to **Bupropion** (a NDRI) or **Mirtazapine** is the preferred clinical strategy.

Q: Which of the following is NOT a TNF-neutralizing agent?

Rituximab. **Explanation:** The question asks to identify the drug that does not neutralize Tumor Necrosis Factor (TNF). **Correct Answer: D. Rituximab** Rituximab is a **chimeric monoclonal antibody directed against the CD20 antigen** found on the surface of B-lymphocytes. It works by depleting B-cells rather than neutralizing TNF-α. It is primarily used in Non-Hodgkin Lymphoma, Chronic Lymphocytic Leukemia (CLL), and severe Rheumatoid Arthritis (RA) refractory to TNF inhibitors. **Why the other options are incorrect (TNF-neutralizing agents):** * **A. Infliximab:** A chimeric monoclonal antibody that binds directly to soluble and transmembrane TNF-α. * **B. Etanercept:** A soluble recombinant **fusion protein** (TNF receptor linked to Fc fraction of IgG1) that acts as a "decoy receptor" to soak up circulating TNF. * **C. Adalimumab:** A fully human monoclonal antibody against TNF-α, which has lower immunogenicity compared to Infliximab. **High-Yield Clinical Pearls for NEET-PG:** 1. **TNF Inhibitors Mnemonic:** "Every Indian Always Gets Certolizumab" (**E**tanercept, **I**nfliximab, **A**dalimumab, **G**olimumab, **C**ertolizumab). 2. **Pre-requisite:** Before starting any TNF inhibitor, patients must be screened for **Latent Tuberculosis** (using TST or IGRA) because TNF is essential for granuloma maintenance; inhibiting it can cause TB reactivation. 3. **Certolizumab pegol** is unique because it is "pegylated" and lacks an Fc portion, reducing placental transfer (safer in pregnancy). 4. **Rituximab Side Effect:** Infusion-related reactions and Progressive Multifocal Leukoencephalopathy (PML) due to JC virus reactivation.

Q: Which of the following agents is not used for the treatment of erectile dysfunction?

Phenylephrine. **Explanation:** The treatment of erectile dysfunction (ED) focuses on increasing blood flow to the *corpora cavernosa* through vasodilation. **Phenylephrine** is a selective **$\alpha_1$-adrenergic agonist** that causes potent vasoconstriction. In the context of male reproductive health, it is used to treat **priapism** (a prolonged, painful erection) by constricting the cavernous arteries and promoting detumescence. Therefore, it is the "odd one out" as it reverses an erection rather than treating ED. **Analysis of Other Options:** * **Vardenafil (Option B):** A selective **PDE-5 inhibitor**. It prevents the breakdown of cGMP, leading to smooth muscle relaxation and increased blood flow. It is a first-line oral treatment for ED. * **Alprostadil (Option D):** This is a synthetic **Prostaglandin E1 (PGE1)** analogue. It increases cAMP levels, causing direct vasodilation. It is administered via intracavernosal injection or intraurethral pellets. * **PGE2 (Option A):** While PGE1 (Alprostadil) is the standard, PGE2 (Dinoprostone) also possesses vasodilatory properties. Historically, it has been used in combination therapies (like "Trimix" or "Quadmix") for ED, though it is more commonly associated with labor induction. **NEET-PG High-Yield Pearls:** 1. **Drug of Choice (DOC) for Priapism:** Intracavernosal Phenylephrine. 2. **PDE-5 Inhibitors Contraindication:** Never co-administer with **Nitrates**, as it can lead to severe, life-threatening hypotension. 3. **Alprostadil Side Effect:** The most common side effect of the injectable form is penile pain and risk of priapism. 4. **Sildenafil (Viagra):** Also used in Pulmonary Arterial Hypertension (PAH).

Question 1

Which of the following statements about protease inhibitors in HIV is false?

Accepted Answer

Of all the protease inhibitors, saquinavir is the most powerful inhibitor of CYP3A4.

Answer

They are powerful enzyme inhibitors.

Answer

They cause hepatic toxicity.

Answer

All protease inhibitors are substrates for P-glycoprotein coded by the MDR gene.

Question 2

Which of the following is responsible for housekeeping functions?

Accepted Answer

COX1

Answer

COX2

Answer

COX3

Answer

All of the above

Question 3

Renal papillary necrosis is commonly caused by which class of drugs?

Accepted Answer

Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)

Answer

Cocaine

Answer

Heroin

Answer

Morphine

Question 4

Allopurinol is used in the treatment of which of the following conditions?

Accepted Answer

Gout

Answer

Osteoarthritis

Answer

Rheumatoid arthritis

Answer

Ankylosing spondylitis

Question 5

What is the best drug for chronic gout in a patient with renal impairment?

Accepted Answer

Naproxen

Answer

Probenecid

Answer

Allopurinol

Answer

Sulfinpyrazone

Question 6

Which of the following is NOT a TNF–α antagonist used in rheumatoid arthritis?

Accepted Answer

Ifosfamide

Answer

Infliximab

Answer

Etanercept

Answer

Adalimumab

Question 7

Which of the following enzymes is inhibited by Aspirin?

Accepted Answer

Cyclooxygenase

Answer

Lipooxygenase

Answer

Phospholipase

Answer

None of the above

Question 8

Which of the following is NOT a side effect of paroxetine?

Accepted Answer

Premature ejaculation

Answer

Erectile dysfunction

Answer

Decreased libido

Answer

Diarrhea

Question 9

Which of the following is NOT a TNF-neutralizing agent?

Accepted Answer

Rituximab

Answer

Infliximab

Answer

Etanercept

Answer

Adalimumab

Question 10

Which of the following agents is not used for the treatment of erectile dysfunction?

Accepted Answer

Phenylephrine

Answer

PGE2

Answer

Vardenafil

Answer

Alprostadil

Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs — MCQs

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