Analgesics and Anti-inflammatory Drugs — MCQs

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

Question 411: Etanercept, used in rheumatoid arthritis, acts by:

A. TNF alpha (Correct Answer)
B. IL-2
C. IL-6
D. TGF beta

Explanation: ***TNF alpha*** - Etanercept is a **fusion protein** that acts as a **decoy receptor** for **TNF-alpha**, binding to it and preventing its interaction with cellular receptors. - By neutralizing **TNF-alpha**, etanercept reduces the inflammation and joint damage associated with **rheumatoid arthritis**. *TGF beta* - **TGF-beta** is a cytokine primarily involved in cell growth, differentiation, and tissue repair, and it generally has an **immunosuppressive role**. - Its mechanism of action is distinct from etanercept, which targets pro-inflammatory pathways. *IL-2* - **IL-2** is a cytokine essential for the proliferation and differentiation of T cells, playing a key role in **adaptive immunity**. - Medications targeting IL-2, such as **daclizumab**, are typically used to prevent transplant rejection or treat certain autoimmune conditions, not rheumatoid arthritis. *IL-6* - **IL-6** is a pro-inflammatory cytokine that contributes significantly to the pathogenesis of rheumatoid arthritis, stimulating acute phase reactants and immune cell activation. - While significant in rheumatoid arthritis, **tocilizumab** (an IL-6 receptor antagonist) targets this pathway, not etanercept.

Question 412: Which of the following drugs is not typically used in the management of acute gout?

A. Colchicine
B. Corticosteroids
C. Sulfinpyrazone (Correct Answer)
D. Non-steroidal anti-inflammatory drugs (NSAIDs)

Explanation: ***Sulfinpyrazone*** - Sulfinpyrazone is a **uricosuric agent** used for **long-term management of chronic gout** by increasing uric acid excretion. - It is not indicated for acute gout attacks as it does not directly address the inflammation and pain experienced during an acute flare. *Non-steroidal anti-inflammatory drugs (NSAIDs)* - NSAIDs like **indomethacin** are cornerstone treatments for acute gout, effectively reducing pain and inflammation. - They work by inhibiting **prostaglandin synthesis**, which mediates the inflammatory response. *Colchicine* - Colchicine is used for **acute gout attacks** as it inhibits neutrophil migration and activity, thereby reducing inflammation. - It is most effective when administered within **24 hours of symptom onset**. *Corticosteroids* - Corticosteroids (e.g., prednisone) are effective anti-inflammatory agents used in acute gout, particularly when NSAIDs are contraindicated. - They can be administered orally, intravenously, or via **intra-articular injection** for rapid relief.

Question 413: Which of the following side effects of opioid analgesics is MOST persistent and does NOT improve with tolerance?

A. Nausea and Vomiting
B. Respiratory Depression
C. Constipation (Correct Answer)
D. Sedation

Explanation: ***Constipation*** - **Opioid-induced constipation** is a very common and persistent side effect due to activation of **opioid receptors** in the gastrointestinal tract, leading to decreased peristalsis and increased water absorption. - Unlike some other side effects, constipation often does not improve over time with continued opioid use and requires proactive management. *Nausea and Vomiting* - While **nausea and vomiting** are common side effects of opioid analgesics, they tend to be more prevalent when initiating therapy or with rapid dose escalation and often improve over time as tolerance develops. - These symptoms are primarily caused by opioid activation of the **chemoreceptor trigger zone** in the brainstem and increased vestibular sensitivity. *Respiratory Depression* - **Respiratory depression** is a serious and potentially life-threatening side effect of opioid analgesics, characterized by decreased respiratory rate and depth. - It is often dose-dependent and a primary concern in opioid overdose, but it is not as universally or persistently experienced as constipation during routine therapeutic use in non-tolerant individuals. *Sedation* - **Sedation** is a common side effect of opioid analgesics, especially when starting treatment or with dose increases, due to their depressant effects on the central nervous system. - Patients often develop tolerance to the sedative effects over time, meaning it becomes less prominent with continued use, unlike opioid-induced constipation.

Question 414: Sufentanil is classified as a potent:

A. Myocardial depressant
B. Analgesic (Correct Answer)
C. Hepatotoxin
D. Anticonvulsant

Explanation: ***Analgesic*** - **Sufentanil** is a synthetic **opioid analgesic** primarily used for its potent pain-relieving effects, especially in surgical and intensive care settings - It acts by binding to and activating **μ-opioid receptors** in the central nervous system, reducing the perception of pain - Approximately **5-10 times more potent than fentanyl**, making it one of the most potent opioid analgesics available - Commonly used in **anesthesia** for its rapid onset and short duration of action *Myocardial depressant* - While high doses of some anesthetic agents can cause myocardial depression, sufentanil has **minimal direct myocardial depressant effects** in clinically relevant doses - Its primary classification is not as a direct cardiac depressant, although it can cause **bradycardia** and hypotension through **vagal stimulation** and decreased sympathetic tone *Hepatotoxin* - There is **no significant evidence** classifying sufentanil as a hepatotoxin that causes liver damage - Liver toxicity is more commonly associated with drugs like **acetaminophen in overdose** or certain anesthetics like **halothane** - Sufentanil is extensively metabolized by the liver but does not cause hepatotoxicity *Anticonvulsant* - **Sufentanil** does not possess anticonvulsant properties - Opioids generally do not have seizure prevention effects and may occasionally lower the seizure threshold, though this is rare with sufentanil at therapeutic doses - Anticonvulsants are a separate class of drugs (e.g., phenytoin, valproate, levetiracetam) used to prevent or reduce seizures

Question 415: Most important side effect of aspirin is?

A. Gastritis (Correct Answer)
B. Edema
C. Kidney damage
D. Hypersensitivity

Explanation: ***Gastritis (and GI toxicity)*** - Aspirin, a **nonsteroidal anti-inflammatory drug (NSAID)**, inhibits **cyclooxygenase (COX) enzymes**, which reduces prostaglandin synthesis [2]. - Reduced prostaglandins in the stomach decrease **mucus production** and **bicarbonate secretion**, leading to mucosal damage and an increased risk of **gastritis, peptic ulcers, and gastrointestinal bleeding** [1]. - This is the **most common and clinically significant** adverse effect of aspirin, occurring in a dose-dependent manner and being the primary reason for discontinuation or requiring gastroprotective co-therapy. *Edema* - While some NSAIDs can cause **fluid retention** and edema by affecting renal function, this is not the most significant or common side effect of aspirin compared to its gastrointestinal effects [2]. - Edema is more prominent with other NSAIDs that have a stronger effect on **renal prostaglandin inhibition**. *Kidney damage* - **Aspirin can be nephrotoxic**, especially in high doses or with prolonged use, by inhibiting renal prostaglandins that regulate blood flow and glomerular filtration [1]. - However, **gastritis and GI bleeding** are generally considered more frequent and severe primary side effects in clinical practice. *Hypersensitivity* - **Aspirin-induced asthma** and other hypersensitivity reactions (like urticaria or angioedema) can occur, especially in individuals with pre-existing asthma or nasal polyps [1]. - While clinically significant, **gastric irritation and bleeding** are more common and are dose-dependent side effects directly related to its mechanism of action.

Question 416: Which of the following is an opioid agonist-antagonist?

A. Pethidine
B. Buprenorphine
C. Methadone
D. Pentazocine (Correct Answer)

Explanation: ***Pentazocine*** - Pentazocine is a **mixed opioid agonist-antagonist**, acting as an agonist at the kappa (κ) opioid receptor and an antagonist or partial agonist at the mu (μ) opioid receptor. - This dual action makes it a **partial analgesic**, but it can also precipitate withdrawal in opioid-dependent individuals. *Pethidine* - Pethidine (meperidine) is a **pure opioid agonist**, primarily acting at the mu (μ) opioid receptor. - It is used for **moderate to severe pain** but is associated with the accumulation of a toxic metabolite, normeperidine, which can cause seizures. *Buprenorphine* - Buprenorphine is a **partial mu (μ) opioid agonist** and a kappa (κ) opioid receptor antagonist. - While it has mixed properties, it is specifically described as a **partial agonist** for its primary analgesic effect, not a typical agonist-antagonist in the same class as pentazocine. *Methadone* - Methadone is a **full opioid agonist** at the mu (μ) opioid receptor, with additional NMDA receptor antagonism and norepinephrine and serotonin reuptake inhibition. - It is known for its **long duration of action** and is primarily used in opioid dependence treatment and chronic pain management.

Question 417: Which among the following is a mechanism of action of colchicine?

A. Decrease in uric acid synthesis
B. None of the options
C. Increase in uric acid excretion
D. Anti-inflammatory action through microtubule disruption (Correct Answer)

Explanation: ***Anti-inflammatory action through microtubule disruption*** - Colchicine works by binding to **tubulin**, thereby inhibiting its polymerization into microtubules. - This disruption of **microtubule formation** in neutrophils and other inflammatory cells prevents their migration and release of inflammatory mediators, thus exerting its anti-inflammatory effect [1].*Increase in uric acid excretion* - Medications that increase uric acid excretion are called **uricosurics**, such as **probenecid**. - Colchicine does not directly affect the renal excretion of uric acid [1].*Decrease in uric acid synthesis* - Medications that decrease uric acid synthesis, like **allopurinol** and **febuxostat**, inhibit the enzyme **xanthine oxidase**. - Colchicine does not inhibit xanthine oxidase and therefore does not reduce uric acid production.*None of the options* - This option is incorrect because **anti-inflammatory action through microtubule disruption** is a well-established mechanism of action for colchicine.

Question 418: Which NSAID has been traditionally and most commonly used for the treatment of acute gout?

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

Explanation: ***Indomethacin*** - Historically, **indomethacin** has been the most frequently prescribed **NSAID** for acute **gouty arthritis** due to its potent anti-inflammatory properties. - It works by inhibiting prostaglandin synthesis, thereby reducing the **inflammation** and **pain** associated with acute gout attacks. - **Note:** While still effective, current guidelines recognize that any NSAID (including naproxen, diclofenac) can be equally effective; the choice depends on patient tolerability and comorbidities. *Aspirin* - **Aspirin** at low doses can actually **raise uric acid levels** by interfering with its renal secretion, potentially exacerbating or prolonging a gout attack. - Therefore, it is generally **contraindicated** for the treatment of acute gout. *Naproxen* - **Naproxen** is an effective NSAID for acute gout with better GI tolerability compared to indomethacin [1]. - Current guidelines consider it equivalent to indomethacin, but **historically**, indomethacin was the classic first-line choice for gout. *Diclofenac* - **Diclofenac** is an NSAID that can be effectively used for acute gout with efficacy similar to other NSAIDs. - While equally effective in current practice, it is not as **historically or classically** associated with gout treatment as **indomethacin**.

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

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