Analgesics and Anti-inflammatory Drugs Practice Questions

Q: Infliximab is directed against which of the following?

Tumor necrosis factor-alpha (TNF-alpha). **Explanation:** **Infliximab** is a chimeric monoclonal antibody (composed of human constant and murine variable regions) that binds with high affinity to both soluble and transmembrane forms of **Tumor Necrosis Factor-alpha (TNF-α)** [2], [3]. By neutralizing TNF-α, it prevents the cytokine from binding to its receptors, thereby inhibiting the downstream inflammatory cascade [3]. This makes it highly effective in treating autoimmune conditions like Rheumatoid Arthritis, Crohn’s disease, and Ankylosing Spondylitis [1], [2]. **Analysis of Incorrect Options:** * **Interleukin-1 (IL-1):** This is the target of **Anakinra** (a recombinant IL-1 receptor antagonist) [2]. * **Interleukin-12 (IL-12):** This, along with IL-23, is targeted by **Ustekinumab**, commonly used in psoriasis and psoriatic arthritis. * **Intercellular Adhesion Molecule (ICAM):** While ICAM-1 is involved in leukocyte trafficking, drugs like **Efalizumab** (now withdrawn) targeted LFA-1 to prevent binding to ICAM, but Infliximab has no direct action here. **High-Yield Clinical Pearls for NEET-PG:** * **TNF-α Inhibitors:** Other examples include **Adalimumab** (fully human mAb) and **Etanercept** (a decoy receptor/fusion protein) [1], [2], [4]. * **Pre-treatment Screening:** Before starting Infliximab, patients **must** be screened for **Latent Tuberculosis** (using TST or IGRA) because TNF-α is essential for granuloma maintenance; inhibiting it can lead to TB reactivation. * **Adverse Effects:** Increased risk of serious infections, infusion reactions, and potential worsening of heart failure [2].

Q: Which of the following is a preferred opioid for pain control in terminally ill cancer patients?

Fentanyl. **Explanation:** **Fentanyl (Option B)** is the preferred opioid for chronic pain management in terminally ill cancer patients, primarily due to its availability as a **transdermal patch**. This delivery system provides continuous, stable analgesia for up to 72 hours, ensuring better patient compliance and avoiding the "peak and valley" effect of oral medications. It is highly lipophilic, potent, and lacks active metabolites, making it safer in patients with renal impairment—a common complication in advanced malignancy. **Why other options are incorrect:** * **Pethidine (Option A):** It is contraindicated for chronic cancer pain. Its metabolite, **norpethidine**, has a long half-life and is neurotoxic, leading to tremors, myoclonus, and seizures, especially with repetitive dosing. * **Methadone (Option C):** While used for chronic pain, it has a very long and unpredictable half-life (15–60 hours), leading to a high risk of cumulative toxicity and respiratory depression. It requires complex titration. * **Remifentanil (Option D):** It has an ultra-short duration of action (metabolized by plasma esterases). It is used exclusively for induction/maintenance of anesthesia via continuous infusion and is unsuitable for long-term outpatient pain control. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC)** for terminal cancer pain (WHO Ladder Step 3): **Morphine** (Oral) is the gold standard; however, **Fentanyl** is the preferred long-term transdermal option. * **Renal Failure:** Fentanyl and Buprenorphine are the safest opioids as they do not have active metabolites excreted by the kidney (unlike Morphine and Hydromorphone). * **Miosis & Constipation:** These are two side effects of opioids to which **tolerance never develops**.

Q: Rasburicase is used in the management of hyperuricemia. By what mechanism does it act?

Increasing urate oxidation. **Mechanism of Action: Rasburicase** **Explanation of the Correct Answer:** Rasburicase is a recombinant form of the enzyme **urate oxidase**. In most mammals, this enzyme converts uric acid into **allantoin**. However, humans lack a functional urate oxidase gene. Rasburicase works by catalyzing the **oxidation** of poorly soluble uric acid into allantoin, which is 5 to 10 times more soluble and easily excreted by the kidneys. This rapidly lowers serum uric acid levels, making it highly effective in preventing and treating Tumor Lysis Syndrome (TLS). **Analysis of Incorrect Options:** * **Option A (Decreasing urate synthesis):** This is the mechanism of **Xanthine Oxidase inhibitors** like Allopurinol and Febuxostat. They prevent the formation of uric acid but do not clear existing uric acid. * **Option C (Decreasing intestinal absorption):** Uric acid is primarily an endogenous metabolic byproduct of purine degradation; intestinal absorption is not a significant target for pharmacological management of hyperuricemia. * **Option D (Increasing renal excretion):** This is the mechanism of **Uricosuric drugs** like Probenecid, Sulfinpyrazone, and Lesinurad, which inhibit the URAT1 transporter in the proximal tubule. **High-Yield Clinical Pearls for NEET-PG:** * **Indication:** Primarily used for the management of hyperuricemia in pediatric and adult patients with leukemia, lymphoma, and solid tumors receiving anti-cancer therapy (Tumor Lysis Syndrome). * **Contraindication:** It is strictly contraindicated in **G6PD deficiency**. The oxidation of uric acid produces **hydrogen peroxide** ($H_2O_2$) as a byproduct, which can trigger severe hemolysis in these patients. * **Pegloticase:** A similar recombinant urate oxidase enzyme, but "pegylated" to increase half-life and decrease immunogenicity; used for refractory chronic gout.

Q: Which of the following disease-modifying antirheumatic drugs (DMARDs) acts by increasing adenosine extracellularly?

Methotrexate. **Explanation:** **Methotrexate (MTX)** is the first-line DMARD for Rheumatoid Arthritis. While it is a dihydrofolate reductase (DHFR) inhibitor at high doses (used in chemotherapy), its anti-inflammatory action at low doses is primarily mediated by **adenosine**. **Mechanism of Action:** Methotrexate inhibits the enzyme **AICAR transformylase**, leading to the intracellular accumulation of AICAR (aminoimidazole carboxamide ribonucleotide). Accumulated AICAR inhibits adenosine deaminase, resulting in an increase in the release of **adenosine** into the extracellular space. Adenosine then acts on **A2A receptors** on inflammatory cells to suppress the production of pro-inflammatory cytokines (like TNF-α and IL-1), thereby exerting its potent anti-inflammatory effect. **Analysis of Incorrect Options:** * **B. Sulfasalazine:** It is broken down into sulfapyridine and 5-ASA. Its mechanism involves inhibiting NF-κB and suppressing cytokine production, but it does not primarily act via adenosine. * **C. Azathioprine:** A prodrug of 6-mercaptopurine, it acts as a purine antimetabolite that inhibits DNA synthesis, primarily affecting T-cell and B-cell proliferation. * **D. Leflunomide:** It inhibits the enzyme **dihydroorotate dehydrogenase (DHODH)**, which blocks *de novo* pyrimidine synthesis, leading to G1 cell cycle arrest in lymphocytes. **High-Yield NEET-PG Pearls:** * **DOC:** Methotrexate is the "Anchor Drug" for Rheumatoid Arthritis. * **Supplementation:** Always co-prescribe **Folic acid** to reduce GI toxicity and mucosal ulcers without compromising efficacy. * **Contraindication:** It is strictly **teratogenic** (causes fetal cranial anomalies) and contraindicated in pregnancy. * **Monitoring:** Watch for hepatotoxicity (monitor LFTs) and pulmonary fibrosis.

Q: Which of the following is a selective cyclo-oxygenase-2 inhibitor?

Nabumetone. **Explanation:** The correct answer is **Nabumetone**. **1. Why Nabumetone is correct:** NSAIDs are classified based on their selectivity for COX enzymes. While most traditional NSAIDs are non-selective, **Nabumetone** is a unique **preferential COX-2 inhibitor**. It is a prodrug converted in the liver to its active metabolite, 6-methoxy-2-naphthylacetic acid (6-MNA). Because it is a non-acidic prodrug and shows greater selectivity for the COX-2 isoform over COX-1, it is associated with a lower incidence of gastrointestinal side effects (like peptic ulcers) compared to traditional NSAIDs. **2. Why other options are incorrect:** * **Ketorolac:** A potent non-selective NSAID with a high affinity for **COX-1**. It is primarily used for short-term management of severe pain due to its high risk of GI toxicity and renal impairment. * **Tolmetin:** An acetic acid derivative and a **non-selective** COX inhibitor used in the treatment of rheumatoid arthritis and osteoarthritis. * **Oxaprozin:** A propionic acid derivative (similar to Ibuprofen) that acts as a **non-selective** COX inhibitor with a long half-life. **3. NEET-PG High-Yield Pearls:** * **Selective COX-2 Inhibitors:** Celecoxib, Etoricoxib, Parecoxib (the "Coxibs"). * **Preferential COX-2 Inhibitors:** Nabumetone, Meloxicam, Etodolac, Nimesulide. * **Clinical Note:** While COX-2 inhibitors spare the GI mucosa, they carry an increased risk of **cardiovascular thrombotic events** (except low-dose aspirin) because they inhibit PGI2 (vasodilator/anti-aggregatory) without affecting TXA2 (vasoconstrictor/pro-aggregatory). * **Nabumetone** is the only non-acidic NSAID in clinical use.

Q: Which of the following is a new oral drug approved for Rheumatoid arthritis?

UPADACITINIB. **Explanation:** **Upadacitinib** is the correct answer as it is a second-generation, oral, selective **Janus Kinase 1 (JAK1) inhibitor** approved for the treatment of moderate-to-severe Rheumatoid Arthritis (RA) in patients who have had an inadequate response to Methotrexate. ### Why Upadacitinib is Correct: In RA, the JAK-STAT signaling pathway plays a crucial role in the release of pro-inflammatory cytokines (like IL-6 and Interferons). While first-generation JAK inhibitors like Tofacitinib target multiple JAK enzymes (JAK1, JAK2, and JAK3), **Upadacitinib** is engineered for greater selectivity toward **JAK1**. This selectivity potentially reduces side effects associated with JAK2 inhibition, such as anemia and thrombocytopenia. ### Analysis of Incorrect Options: * **B. Fedratinib:** This is a selective **JAK2 inhibitor** primarily used in the treatment of **Myelofibrosis**, not RA. * **C. Entrectinib:** This is a tyrosine kinase inhibitor (TKI) targeting **NTRK and ROS1**, used as an anti-cancer agent for solid tumors and non-small cell lung cancer (NSCLC). * **D. Talazoparib:** This is a **PARP inhibitor** used in the treatment of BRCA-mutated HER2-negative breast cancer. ### High-Yield Clinical Pearls for NEET-PG: * **JAK Inhibitor Suffix:** Drugs ending in **"-tinib"** are generally tyrosine kinase inhibitors. * **Other JAK Inhibitors in RA:** Tofacitinib (Pan-JAK), Baricitinib (JAK1/2), and Filgotinib (JAK1). * **Route of Administration:** Unlike biological DMARDs (e.g., Adalimumab, Etanercept) which are injectable, JAK inhibitors are **orally administered**. * **Pre-treatment Screening:** Always screen for **Latent Tuberculosis** and Hepatitis B/C before starting JAK inhibitors, as they can cause reactivation.

Q: What is the recommended dose of methotrexate for the treatment of rheumatoid arthritis?

7.5 - 15 mg per week. **Explanation:** Methotrexate (MTX) is the "anchor drug" and the first-line Disease-Modifying Antirheumatic Drug (DMARD) for Rheumatoid Arthritis (RA). In RA, it acts primarily by inhibiting **aminoimidazolecarboxamide ribonucleotide (AICAR) transformylase**, leading to increased extracellular adenosine, which has potent anti-inflammatory effects. **Why Option A is Correct:** The standard starting dose for RA is **7.5 to 15 mg administered once weekly**. This dose is significantly lower than those used in cancer chemotherapy because the goal is immunomodulation rather than cytotoxicity. The dose can be escalated up to 25 mg/week based on patient response and tolerance. **Why Other Options are Incorrect:** * **Options B & D (2.5 - 5 mg):** These doses are sub-therapeutic for RA and would fail to achieve adequate disease control. * **Options C & D (Monthly dosing):** Methotrexate has a relatively short half-life; monthly administration would not maintain the steady-state concentration required to suppress chronic synovial inflammation. **Weekly dosing** is the gold standard to balance efficacy with safety. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism (Low dose):** Increases adenosine (anti-inflammatory). * **Mechanism (High dose/Onco):** Inhibits **Dihydrofolate Reductase (DHFR)**, preventing DNA synthesis. * **Supplementation:** Always co-prescribe **Folic acid (5 mg)** to reduce GI side effects, mucosal ulcers, and hepatotoxicity without compromising efficacy. * **Monitoring:** Regular Liver Function Tests (LFTs) and CBC are mandatory due to risks of hepatotoxicity and bone marrow suppression. * **Contraindication:** It is highly **teratogenic** (Category X); it must be stopped at least 3 months before conception in both males and females.

Question 1

True regarding morphine?

Accepted Answer

Tolerance develops for all effects except miosis and constipation.

Answer

Tolerance to all effects develops with chronic usage.

Answer

Tolerance develops for all effects except euphoria and sedation.

Answer

Tolerance can develop to all effects in high doses.

Question 2

Infliximab is directed against which of the following?

Accepted Answer

Tumor necrosis factor-alpha (TNF-alpha)

Answer

Interleukin-1 (IL-1)

Answer

Interleukin-12 (IL-12)

Answer

Intercellular adhesion molecule (ICAM)

Question 3

Which of the following is a preferred opioid for pain control in terminally ill cancer patients?

Accepted Answer

Fentanyl

Answer

Pethidine

Answer

Methadone

Answer

Remifentanyl

Question 4

Aspirin protects against which of the following conditions?

Accepted Answer

Liver cancer

Answer

Myocardial infarction

Answer

Stroke

Answer

Colorectal cancer

Question 5

Rasburicase is used in the management of hyperuricemia. By what mechanism does it act?

Accepted Answer

Increasing urate oxidation

Answer

Decreasing urate synthesis

Answer

Decreasing intestinal absorption of uric acid

Answer

Increasing renal excretion of uric acid

Question 6

Which of the following disease-modifying antirheumatic drugs (DMARDs) acts by increasing adenosine extracellularly?

Accepted Answer

Methotrexate

Answer

Sulfasalazine

Answer

Azathioprine

Answer

Leflunomide

Question 7

All of the following effects are produced by inhibitors of prostaglandin synthesis EXCEPT:

Accepted Answer

Prolongation of prothrombin time

Answer

Prolongation of bleeding time

Answer

Prolongation of labour

Answer

Gastric mucosal damage

Question 8

Which of the following is a selective cyclo-oxygenase-2 inhibitor?

Accepted Answer

Nabumetone

Answer

Ketorolac

Answer

Tolmetin

Answer

Oxaprozin

Question 9

Which of the following is a new oral drug approved for Rheumatoid arthritis?

Accepted Answer

UPADACITINIB

Answer

FEDRATINIB

Answer

ENTRECTINIB

Answer

TALAZOPARIB

Question 10

What is the recommended dose of methotrexate for the treatment of rheumatoid arthritis?

Accepted Answer

7.5 - 15 mg per week

Answer

2.5 - 5 mg per week

Answer

7.5 - 15 mg per month

Answer

2.5 - 5 mg per month

Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs — MCQs

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