Analgesics and Anti-inflammatory Drugs Practice Questions

Q: Which of the following features differentiates pethidine from morphine?

Local anaesthetic action. **Explanation:** **Pethidine (Meperidine)** is a synthetic opioid agonist that, while sharing the same primary mechanism of action as morphine (µ-opioid receptor agonism), possesses distinct pharmacological properties due to its unique chemical structure. 1. **Why Option A is Correct:** Unlike morphine, pethidine possesses significant **local anaesthetic properties**. It can block sodium channels, a feature not seen with morphine. Clinically, this is relevant because pethidine can be used for spinal anesthesia, providing both sensory and motor blockade, although it is rarely used this way due to the availability of better agents. 2. **Why Incorrect Options are Wrong:** * **Option B:** Pethidine is **less potent** than morphine. Approximately 75–100 mg of pethidine is required to produce the same analgesic effect as 10 mg of morphine. * **Option C:** Pethidine causes **less respiratory depression** in the newborn compared to morphine when used during labor, making it a preferred choice in obstetric analgesia (though it is not entirely risk-free). * **Option D:** Pethidine has **negligible antitussive (cough suppressant) action**. Morphine and its derivatives (like codeine) are potent cough suppressants. **High-Yield Clinical Pearls for NEET-PG:** * **Anticholinergic Activity:** Pethidine has atropine-like effects, leading to **mydriasis** (unlike morphine's miosis) and tachycardia. * **Toxic Metabolite:** It is metabolized to **norpethidine**, which is a CNS stimulant. Accumulation (especially in renal failure) can lead to **seizures**. * **Drug Interaction:** Pethidine is contraindicated with **MAO inhibitors**, as it can precipitate a life-threatening "Serotonin Syndrome" (hyperpyrexia, coma, and convulsions). * **Smooth Muscle:** It causes less spasm of the Sphincter of Oddi compared to morphine, making it historically preferred for biliary colic.

Q: What is the antagonist of morphine?

Naloxone. **Explanation:** **1. Why Naloxone is the Correct Answer:** Naloxone is a **pure opioid antagonist** that competes with opioids at all three receptor sites ($\mu$, $\kappa$, and $\delta$), with the highest affinity for $\mu$-receptors. It is the drug of choice for treating acute opioid overdose because it rapidly reverses respiratory depression and sedation. Due to its extensive first-pass metabolism, it is administered parenterally (IV/IM) and has a short duration of action (30–90 minutes), often requiring repeated doses. **2. Analysis of Incorrect Options:** * **Nalbuphine:** This is a **mixed agonist-antagonist** ($\kappa$-agonist and $\mu$-antagonist). While it can reverse $\mu$-mediated respiratory depression, it possesses intrinsic analgesic activity and is not used as a primary antagonist. * **Nalorphine:** This was the first opioid antagonist discovered but is also a **mixed agonist-antagonist**. It is rarely used today because it can cause unpleasant psychotomimetic side effects (dysphoria, hallucinations) via $\kappa$-receptor activation. * **Methadone:** This is a **full $\mu$-agonist** with a long half-life. It is used in the management of opioid detoxification and maintenance programs to prevent withdrawal symptoms, not to antagonize morphine. **3. High-Yield Clinical Pearls for NEET-PG:** * **Naltrexone:** Unlike Naloxone, Naltrexone is orally active and long-acting. It is used for **maintenance** in detoxified addicts and to reduce alcohol cravings. * **Methylnaltrexone/Alvimopan:** These are peripheral opioid antagonists used to treat opioid-induced constipation without reversing central analgesia. * **Diagnostic Sign:** In morphine poisoning, look for the triad of **Pinpoint pupil (miosis)**, **Respiratory depression**, and **Coma**. Naloxone will cause immediate pupillary dilation and arousal.

Q: Aspirin is contraindicated in children suffering from influenza or similar viral infections due to an increased risk of which condition?

Reye's syndrome. ### Explanation **Correct Option: D. Reye's Syndrome** Reye’s syndrome is a rare but potentially fatal condition characterized by **acute encephalopathy** and **fatty degeneration of the liver (microvesicular steatosis)**. The pathophysiology involves mitochondrial injury, which is triggered when aspirin is administered to children or adolescents during a viral prodrome (typically Influenza A, B, or Varicella). Aspirin inhibits mitochondrial beta-oxidation, leading to hyperammonemia and cerebral edema. Therefore, **Acetaminophen (Paracetamol)** is the preferred antipyretic in the pediatric population. **Analysis of Incorrect Options:** * **A. Fanconi Syndrome:** This is a disorder of the proximal renal tubules resulting in the excretion of glucose, amino acids, and phosphates. While associated with expired tetracyclines or heavy metal poisoning, it is not linked to aspirin use in viral infections. * **B. Thrombocytopenia:** While aspirin inhibits platelet aggregation (via irreversible COX-1 inhibition), it does not typically cause a decrease in the absolute platelet count (thrombocytopenia). * **C. Gastric Bleeding:** Aspirin is a known cause of gastric mucosal injury and GI bleeding due to the inhibition of protective prostaglandins ($PGE_2$). However, this is a general side effect and not the specific reason for its contraindication in pediatric viral illnesses. **High-Yield Clinical Pearls for NEET-PG:** * **Exception to the rule:** Aspirin is still used in children for **Kawasaki Disease** (to prevent coronary artery aneurysms) and **Juvenile Idiopathic Arthritis**, despite the risk of Reye's syndrome. * **Histology:** Look for "microvesicular steatosis" in liver biopsy descriptions for Reye's syndrome. * **Salicylism:** Chronic aspirin toxicity presents with tinnitus, vertigo, and a mixed respiratory alkalosis/metabolic acidosis.

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

Leflunomide. **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.

Q: Morphine causes all of the following effects, except:

Decrease in intracranial tension. **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).

Q: Which of the following is a partial agonist of opioids?

Buprenorphine. **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.

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

Acute gouty arthritis. **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.

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

Parecoxib. **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).

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

Indomethacin. **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].

Q: 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?

Allopurinol. **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 1

Which of the following features differentiates pethidine from morphine?

Accepted Answer

Local anaesthetic action

Answer

More analgesic action

Answer

More respiratory depression

Answer

Suppresses cough effectively

Question 2

What is the antagonist of morphine?

Accepted Answer

Naloxone

Answer

Nalbuphine

Answer

Nalorphine

Answer

Methadone

Question 3

Aspirin is contraindicated in children suffering from influenza or similar viral infections due to an increased risk of which condition?

Accepted Answer

Reye's syndrome

Answer

Fanconi syndrome

Answer

Thrombocytopenia

Answer

Gastric bleeding

Question 4

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

Accepted Answer

Leflunomide

Answer

Sulfasalazine

Answer

Nimesulide

Answer

Colchicine

Question 5

Morphine causes all of the following effects, except:

Accepted Answer

Decrease in intracranial tension

Answer

Peripheral vasodilation

Answer

Nausea and vomiting

Answer

Decrease in gastrointestinal secretion

Question 6

Which of the following is a partial agonist of opioids?

Accepted Answer

Buprenorphine

Answer

Pethidine

Answer

Morphine

Answer

Butorphanol

Question 7

Allopurinol is useful in all of the following conditions EXCEPT?

Accepted Answer

Acute gouty arthritis

Answer

Cancer chemotherapy induced hyperuricemia

Answer

Hydrochlorothiazide induced hyperuricemia

Answer

Kala azar

Question 8

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

Accepted Answer

Parecoxib

Answer

Diflunisal

Answer

Piroxicam

Answer

Sulindac

Question 9

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

Accepted Answer

Indomethacin

Answer

Celecoxib

Answer

Naproxen

Answer

Diclofenac sodium

Question 10

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?

Accepted Answer

Allopurinol

Answer

Aspirin

Answer

Colchicine

Answer

Hydroxychloroquine

Analgesics and Anti-inflammatory Drugs — MCQs

Analgesics and Anti-inflammatory Drugs — MCQs

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