Analgesics and Anti-inflammatory Drugs — MCQs

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

Question 91: Infliximab (systemic) is used in which of the following conditions?

A. Crohn's disease (treatment)
B. To reduce the number of draining enterocutaneous fistulas in patients with fistulizing Crohn's disease
C. Rheumatoid arthritis (treatment)
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Infliximab** is a chimeric monoclonal antibody (composed of human and murine regions) that acts as a potent **TNF-α (Tumor Necrosis Factor-alpha) inhibitor**. TNF-α is a key pro-inflammatory cytokine involved in the pathogenesis of several chronic inflammatory and autoimmune conditions. **Why "All of the above" is correct:** * **Crohn’s Disease (Option A & B):** Infliximab is highly effective in inducing and maintaining remission in moderate-to-severe Crohn’s disease. Specifically, it is the gold standard for treating **fistulizing Crohn’s disease**, as it promotes the closure of enterocutaneous fistulas and reduces their drainage. * **Rheumatoid Arthritis (Option C):** It is used in patients with moderate-to-severe RA who have had an inadequate response to methotrexate. It is typically administered in combination with methotrexate to prevent the formation of human anti-chimeric antibodies (HACAs), which can decrease the drug's efficacy. **Clinical Pearls for NEET-PG:** 1. **Mechanism:** It binds to both soluble and transmembrane forms of TNF-α, preventing them from binding to their receptors. 2. **Pre-treatment Screening:** Before starting Infliximab, patients **must** be screened for **Latent Tuberculosis (TB)** using a TST or IGRA, as TNF inhibitors can cause the reactivation of TB. 3. **Other Indications:** Ulcerative colitis, Ankylosing spondylitis, Psoriatic arthritis, and Plaque psoriasis. 4. **Contraindications:** It should be avoided in patients with New York Heart Association (NYHA) Class III or IV **heart failure**, as it can worsen the condition. 5. **Route:** Unlike many other TNF inhibitors (like Etanercept or Adalimumab which are subcutaneous), Infliximab is administered via **Intravenous (IV) infusion**.

Question 92: Which disease-modifying antirheumatic drug's active metabolite inhibits the enzyme dihydro-orotate dehydrogenase?

A. Sulfasalazine
B. Nimesulide
C. Leflunomide (Correct Answer)
D. Colchicine

Explanation: **Explanation:** **Leflunomide** is a Disease-Modifying Antirheumatic Drug (DMARD) used primarily in the treatment of Rheumatoid Arthritis. It acts as a prodrug and is rapidly converted in the gut and plasma to its active metabolite, **A77 1726 (teriflunomide)**. **Mechanism of Action:** The active metabolite inhibits the mitochondrial enzyme **dihydro-orotate dehydrogenase (DHODH)**. This enzyme is critical for the *de novo* synthesis of pyrimidines (specifically UMP). Since activated T-lymphocytes depend on *de novo* synthesis to proliferate (unlike other cells which use the salvage pathway), leflunomide effectively arrests these cells in the G1 phase, reducing the autoimmune inflammatory response. **Analysis of Incorrect Options:** * **A. Sulfasalazine:** A DMARD that is broken down into sulfapyridine and 5-ASA. Its exact mechanism in RA is unclear but involves inhibition of cytokine release (IL-1, TNF-α); it does not inhibit DHODH. * **B. Nimesulide:** A selective COX-2 inhibitor (NSAID) used for acute pain and inflammation. It does not have disease-modifying properties. * **C. Colchicine:** Used in gout, it inhibits microtubule polymerization by binding to tubulin, interfering with leukocyte migration and phagocytosis. **High-Yield Clinical Pearls for NEET-PG:** * **Loading Dose:** Due to its long half-life (~2 weeks), a loading dose was traditionally used, though often skipped now to reduce GI toxicity. * **Side Effects:** Hepatotoxicity (monitor LFTs) and alopecia are common. It is highly **teratogenic**. * **Washout Procedure:** If pregnancy is desired or toxicity occurs, **Cholestyramine** is administered to enhance fecal excretion via interruption of enterohepatic circulation.

Question 93: Morphine causes all of the following effects, except:

A. Peripheral vasodilation
B. Decrease in intracranial tension (Correct Answer)
C. Nausea and vomiting
D. Decrease in gastrointestinal secretion

Explanation: **Explanation:** The correct answer is **B. Decrease in intracranial tension**. In fact, Morphine **increases** intracranial pressure (ICP). **Mechanism of Increased ICP:** Morphine causes respiratory depression by reducing the sensitivity of the brainstem respiratory center to $CO_2$. This leads to $CO_2$ retention (hypercapnia). Elevated $CO_2$ levels act as a potent cerebral vasodilator, increasing cerebral blood flow and subsequently raising intracranial tension. This is a critical clinical contraindication: Morphine should be avoided in patients with head injuries. **Analysis of Incorrect Options:** * **A. Peripheral vasodilation:** Morphine triggers the release of histamine from mast cells and has a direct effect on vascular smooth muscle, leading to peripheral vasodilation and potential hypotension. * **C. Nausea and vomiting:** Morphine directly stimulates the Chemoreceptor Trigger Zone (CTZ) in the area postrema of the medulla, commonly causing emesis in ambulatory patients. * **D. Decrease in gastrointestinal secretion:** Morphine acts on $\mu$-receptors in the gut to decrease gastric, biliary, and pancreatic secretions. It also increases sphincter tone and decreases intestinal motility, leading to its well-known side effect of constipation. **High-Yield NEET-PG Pearls:** * **Miosis (Pin-point pupil):** Occurs via stimulation of the Edinger-Westphal nucleus. Unlike other effects, tolerance does *not* develop to miosis or constipation. * **Biliary Colic:** Morphine causes constriction of the Sphincter of Oddi; therefore, it is generally avoided in biliary colic (Pethidine is often preferred as it has less effect on the sphincter). * **Triad of Opioid Overdose:** Coma, Pin-point pupil, and Respiratory depression. * **Antidote:** Naloxone (pure antagonist).

Question 94: Which of the following is a partial agonist of opioids?

A. Pethidine
B. Buprenorphine (Correct Answer)
C. Morphine
D. Butorphanol

Explanation: **Explanation:** **Buprenorphine** is the correct answer because it is a **partial mu (μ) opioid agonist** and a kappa (κ) antagonist. As a partial agonist, it has high affinity for the μ-receptor but low intrinsic activity. This results in a "ceiling effect," where increasing the dose beyond a certain point does not increase respiratory depression or euphoria, making it safer than full agonists. **Analysis of Incorrect Options:** * **A. Pethidine (Meperidine):** A full μ-agonist. It is notable for its metabolite, *normeperidine*, which can cause seizures, and its lack of miosis (it causes mydriasis due to its atropine-like structure). * **C. Morphine:** The prototype full μ-opioid agonist. It has high intrinsic activity at μ-receptors and is the standard against which other opioids are compared. * **D. Butorphanol:** This is an **agonist-antagonist**, specifically a κ-agonist and a μ-antagonist (or very weak partial agonist). It is distinct from buprenorphine, which is primarily a partial μ-agonist. **High-Yield NEET-PG Pearls:** 1. **Ceiling Effect:** Buprenorphine exhibits a ceiling effect for respiratory depression, making it useful in opioid substitution therapy (maintenance) for addiction. 2. **Precipitated Withdrawal:** If buprenorphine is given to a patient physically dependent on a full agonist (like Morphine), it can displace the full agonist and precipitate withdrawal symptoms. 3. **Naloxone Resistance:** Due to its very high receptor affinity, buprenorphine-induced respiratory depression is difficult to reverse with standard doses of Naloxone. 4. **Drug of Choice:** Buprenorphine is often preferred over Methadone for office-based addiction treatment due to its better safety profile.

Question 95: Allopurinol is useful in all of the following conditions EXCEPT?

A. Cancer chemotherapy induced hyperuricemia
B. Hydrochlorothiazide induced hyperuricemia
C. Acute gouty arthritis (Correct Answer)
D. Kala azar

Explanation: **Explanation:** The correct answer is **C. Acute gouty arthritis**. **1. Why Allopurinol is contraindicated in Acute Gout:** Allopurinol is a **Xanthine Oxidase inhibitor** that reduces the synthesis of uric acid. However, it should never be started during an acute attack of gout. Rapidly lowering serum urate levels causes the mobilization of urate crystals from joint tissues into the synovial fluid. This "re-shuffling" of crystals triggers further inflammation, potentially worsening or prolonging the acute episode. In acute gout, the treatment of choice is **NSAIDs** (e.g., Indomethacin), **Colchicine**, or **Corticosteroids**. Allopurinol is reserved for chronic prophylaxis *after* the acute inflammation has subsided. **2. Analysis of Incorrect Options:** * **A. Cancer chemotherapy:** Rapid cell lysis (Tumor Lysis Syndrome) leads to massive purine release and hyperuricemia. Allopurinol is standard prophylaxis to prevent urate nephropathy. * **B. Hydrochlorothiazide induced hyperuricemia:** Thiazide diuretics compete with uric acid for excretion in the renal tubules, leading to secondary hyperuricemia. Allopurinol effectively manages this elevation. * **D. Kala-azar:** Allopurinol is used as an adjuvant/alternative treatment for Leishmaniasis. The *Leishmania* parasite cannot synthesize purines de novo and incorporates allopurinol into its RNA, which inhibits its growth. **High-Yield Clinical Pearls for NEET-PG:** * **Drug Interaction:** Allopurinol inhibits the metabolism of **6-Mercaptopurine** and **Azathioprine**. If co-administered, the dose of these immunosuppressants must be reduced by 75%. * **Hypersensitivity:** Watch for **Stevens-Johnson Syndrome (SJS)**, especially in patients with the **HLA-B*5801** allele. * **Febuxostat:** A non-purine selective inhibitor of xanthine oxidase used in patients intolerant to Allopurinol.

Question 96: Which of the following is a selective COX-2 inhibitor?

A. Diflunisal
B. Piroxicam
C. Sulindac
D. Parecoxib (Correct Answer)

Explanation: **Explanation:** **1. Why Parecoxib is correct:** NSAIDs are classified based on their selectivity for Cyclooxygenase (COX) enzymes. **Parecoxib** is a prodrug of Valdecoxib and belongs to the "Coxib" class, which specifically targets the **COX-2 isoenzyme**. COX-2 is primarily induced at sites of inflammation, whereas COX-1 is constitutive and responsible for gastric protection and platelet function. By selectively inhibiting COX-2, Parecoxib provides potent analgesia and anti-inflammatory effects with a significantly lower risk of gastrointestinal ulcers compared to non-selective NSAIDs. Notably, Parecoxib is the only selective COX-2 inhibitor available for **parenteral (injectable) administration**, making it useful for postoperative pain management. **2. Why the other options are incorrect:** * **Diflunisal (A):** A salicylic acid derivative. It is a **non-selective** inhibitor of both COX-1 and COX-2. * **Piroxicam (B):** An oxicam derivative known for its long half-life. It is a **non-selective** NSAID and is associated with a high risk of GI side effects. * **Sulindac (C):** An acetic acid derivative and a prodrug. It is a **non-selective** inhibitor. It is often noted for being "renal-sparing" as it has less effect on renal prostaglandins. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cardiovascular Risk:** While selective COX-2 inhibitors protect the stomach, they increase the risk of thrombotic events (MI/Stroke) because they inhibit PGI2 (vasodilator/anti-aggregatory) without affecting Thromboxane A2 (vasoconstrictor/pro-aggregatory). * **Sulfonamide Allergy:** Most Coxibs (except Etoricoxib) contain a sulfonamide moiety and should be used cautiously in patients with sulfa allergies. * **Etoricoxib:** The most COX-2 selective agent among the available Coxibs. * **Celecoxib:** The only Coxib currently approved for reducing colonic polyps in Familial Adenomatous Polyposis (FAP).

Question 97: Which of the following NSAIDs should not be prescribed to a patient with a minor soft tissue injury?

A. Celecoxib
B. Indomethacin (Correct Answer)
C. Naproxen
D. Diclofenac sodium

Explanation: **Explanation:**The correct answer is **Indomethacin**.**Why Indomethacin is the correct choice:**Indomethacin is one of the most potent non-selective COX inhibitors. While highly effective, it is associated with a **high incidence of systemic adverse effects** (occurring in 30–50% of patients) [1], including severe frontal headaches, dizziness, GI bleeding, and bone marrow suppression. In clinical practice, its use is reserved for "high-intensity" inflammatory conditions such as **acute gouty arthritis, ankylosing spondylitis, and patent ductus arteriosus (PDA)** [1]. For a minor soft tissue injury, the risk-to-benefit ratio does not justify its use when safer alternatives are available.**Analysis of Incorrect Options:** * **Celecoxib:** A selective COX-2 inhibitor. It is preferred in patients with a high risk of peptic ulcers and is appropriate for musculoskeletal pain where traditional NSAIDs might cause GI distress. * **Naproxen:** A propionic acid derivative with a relatively better cardiovascular safety profile compared to other NSAIDs. It is a standard choice for minor injuries and long-term management of musculoskeletal pain. * **Diclofenac sodium:** One of the most commonly prescribed NSAIDs for soft tissue injuries and inflammation due to its good analgesic potency and accumulation in synovial fluid.**High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Indomethacin is the DOC for **Ankylosing Spondylitis** and **Bartter syndrome** [1]. * **PDA:** Indomethacin (or Ibuprofen/Paracetamol) is used to close a Patent Ductus Arteriosus [1]. * **Ophthalmic use:** Indomethacin eye drops are used to prevent miosis during cataract surgery. * **Contraindication:** Avoid Indomethacin in patients with psychiatric disorders, epilepsy, or renal impairment due to its CNS and renal side effects [1].

Question 98: A patient with known gout presents with elevated serum uric acid. Which of the following drugs is most suitable for chronic therapy to lower uric acid levels?

A. Aspirin
B. Colchicine
C. Allopurinol (Correct Answer)
D. Hydroxychloroquine

Explanation: **Explanation:** The management of gout is divided into two phases: treatment of acute attacks and chronic management of hyperuricemia. **1. Why Allopurinol is Correct:** Allopurinol is the drug of choice for the **chronic management** of gout. It is a **Xanthine Oxidase inhibitor** that acts by reducing the synthesis of uric acid. It is a purine analog that competitively inhibits the enzyme xanthine oxidase, which is responsible for converting hypoxanthine to xanthine and xanthine to uric acid. By lowering serum urate levels below the saturation point, it prevents the formation of new urate crystals and allows existing tophi to dissolve. **2. Why the Other Options are Incorrect:** * **Aspirin:** In low doses, aspirin inhibits the tubular secretion of uric acid, leading to hyperuricemia. While high-dose aspirin is uricosuric, it is not used clinically for gout due to toxicity. * **Colchicine:** This is primarily used for the treatment of **acute gouty arthritis** and for prophylaxis during the initiation of urate-lowering therapy. It inhibits microtubule polymerization (binding to tubulin) but does not lower serum uric acid levels. * **Hydroxychloroquine:** This is a Disease-Modifying Antirheumatic Drug (DMARD) used in Rheumatoid Arthritis and SLE; it has no role in the management of gout. **Clinical Pearls for NEET-PG:** * **HLA-B*5801:** Screening is recommended in certain populations (e.g., Han Chinese, Thai) before starting Allopurinol to prevent **Stevens-Johnson Syndrome (SJS)/Toxic Epidermal Necrolysis (TEN)**. * **Acute Flare:** Never start Allopurinol during an acute attack, as sudden changes in urate levels can worsen the inflammation. Always co-prescribe NSAIDs or Colchicine when initiating therapy. * **Febuxostat:** A non-purine selective inhibitor of xanthine oxidase used if Allopurinol is not tolerated.

Question 99: Which of the following opioids has the most potent analgesic effect?

A. Morphine
B. Fentanyl
C. Sufentanil (Correct Answer)
D. Meperidine

Explanation: The correct answer is **Sufentanil**. The potency of an opioid is determined by its affinity for the mu (μ) opioid receptors and its lipid solubility. **Why Sufentanil is correct:** Sufentanil is a thienyl analogue of fentanyl and is currently the most potent opioid analgesic used in clinical practice [1]. It is approximately **5 to 10 times more potent than fentanyl** and nearly **500 to 1,000 times more potent than morphine** [1]. Its high lipid solubility allows it to cross the blood-brain barrier rapidly, providing an immediate and intense analgesic effect, primarily used in cardiac anesthesia and critical care. **Analysis of Incorrect Options:** * **Morphine:** The prototype opioid against which others are measured (potency = 1). While effective, it is significantly less potent than the synthetic phenylpiperidine derivatives like fentanyl or sufentanil [1, 2]. * **Fentanyl:** A highly potent synthetic opioid (approx. 100 times more potent than morphine). While very strong, it is surpassed in potency by its derivative, sufentanil [1]. * **Meperidine (Pethidine):** This is much less potent than morphine (approx. 1/10th the potency) [1]. It is notable for its metabolite, normeperidine, which can cause seizures. **High-Yield NEET-PG Pearls:** * **Potency Order:** Sufentanil > Remifentanil > Fentanyl > Alfentanil > Morphine > Meperidine [1, 2]. * **Remifentanil:** Unique for its metabolism by **plasma cholinesterases**, giving it an ultra-short half-life (not dependent on liver/kidney function). * **Clinical Note:** Sufentanil is preferred in cardiac surgeries because it provides excellent hemodynamic stability.

Question 100: Which of the following is NOT produced by mu receptors?

A. Euphoria
B. Sedation
C. Dysphoria (Correct Answer)
D. Constipation

Explanation: **Explanation:** The correct answer is **Dysphoria** because it is a characteristic effect of **Kappa (κ) opioid receptors**, not Mu (μ) receptors. **1. Why Dysphoria is the correct answer:** Opioid receptors are classified into three main types: Mu (μ), Kappa (κ), and Delta (δ). While **Mu receptors** are associated with feelings of well-being and **Euphoria** (due to dopamine release in the nucleus accumbens), **Kappa receptors** produce the opposite effect, known as **Dysphoria** (feelings of unease or dissatisfaction) and psychotomimetic effects (hallucinations). **2. Analysis of Incorrect Options:** * **Euphoria (A):** This is a hallmark effect of Mu receptor activation. It contributes to the high abuse potential of opioids like morphine and heroin. * **Sedation (B):** Mu receptors mediate central nervous system depression, leading to drowsiness and sedation. (Note: Kappa receptors also cause sedation, but it is a primary feature of Mu activation). * **Constipation (C):** Mu receptors are highly concentrated in the myenteric plexus of the gastrointestinal tract. Their activation inhibits peristalsis, making constipation one of the most common and persistent side effects of Mu-agonists. **Clinical Pearls for NEET-PG:** * **Mu (μ) Receptors:** Responsible for Supraspinal analgesia, Respiratory depression (most dangerous side effect), Miosis (pinpoint pupil), and Physical dependence. * **Kappa (κ) Receptors:** Responsible for Spinal analgesia, Dysphoria, and Diuresis (by inhibiting ADH). * **Delta (δ) Receptors:** Primarily involved in spinal/supraspinal analgesia and modulating Mu receptor activity. * **Mnemonic:** **M**u = **M**ore **M**iosis, **M**ore Euphoria; **K**appa = **K**eep out (Dysphoria/Hallucinations).

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

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Migraine Therapeutics

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Neuropathic Pain Management

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