Analgesics and Anti-inflammatory Drugs — MCQs

A 50-year-old man presents with complaints of bilateral morning stiffness in his wrists and knees and painful joints on exercise. On physical examination, the joints are slightly swollen. The rest of the examination is unremarkable. His laboratory findings are also negative except for slight anemia, elevated erythrocyte sedimentation rate, and positive rheumatoid factor. The patient was started on weekly methotrexate to control the inflammation. What is the principle mechanism of action here?

Q379

All are opioid agonist - antagonist compounds except

Q380

Morphine should not be used in the treatment of:

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

Question 371: The primary goal of glucocorticoid treatment in rheumatoid arthritis is -

A. Suppression of inflammation and improvement in functional capacity (Correct Answer)
B. Prevention of suppression of the hypothalamic pituitary-adrenal axis
C. Development of a sense of well-being in the patient
D. Reversal of the degenerative process

Explanation: ***Suppression of inflammation and improvement in functional capacity*** - **Glucocorticoids** are potent anti-inflammatory agents that rapidly reduce pain, swelling, and stiffness in **rheumatoid arthritis (RA)**. - This reduction in inflammation directly leads to improved **joint function** and overall quality of life for the patient. *Prevention of suppression of the hypothalamic pituitary-adrenal axis* - **Suppression of the HPA axis** is an *undesirable side effect* of chronic glucocorticoid use, not a primary goal of treatment. - While clinicians try to minimize this, it is a complication to manage, not an intended therapeutic effect. *Development of a sense of well-being in the patient* - While patients often experience an improved sense of well-being due to rapid symptom relief, this is a **secondary outcome** of effective inflammation control. - The direct objective of the medication is physiological—targeting the inflammatory process. *Reversal of the degenerative process* - Glucocorticoids do not reverse the **structural damage** or **degenerative changes** to joints that occur in chronic RA. - Their main role is to control the inflammatory component, which helps prevent further damage but does not repair existing erosion.

Question 372: A drug that is effective for rheumatoid arthritis but is not appropriate for osteoarthritis is :

A. Infliximab (Correct Answer)
B. Rofecoxib
C. Acetaminophen
D. Ketorolac

Explanation: ***Infliximab*** - **Infliximab** is a **biologic disease-modifying antirheumatic drug (DMARD)**, specifically a TNF-alpha inhibitor, used to treat **autoimmune inflammatory conditions** like rheumatoid arthritis. - Its mechanism involves modulating the immune system to reduce inflammation, which is not applicable to the **degenerative process** seen in osteoarthritis. *Rofecoxib* - **Rofecoxib** was a **COX-2 selective NSAID** used for pain and inflammation in both rheumatoid arthritis and osteoarthritis. - It was withdrawn from the market due to increased cardiovascular risk, but its initial indication covered both conditions for symptomatic relief. *Acetaminophen* - **Acetaminophen** (paracetamol) is an **analgesic** and **antipyretic** primarily used for pain relief in both osteoarthritis and rheumatoid arthritis. - It does not have significant anti-inflammatory properties and therefore is not a disease-modifying agent for rheumatoid arthritis. *Ketorolac* - **Ketorolac** is a potent **non-selective NSAID** commonly used for **acute pain** of moderate to severe intensity. - It provides symptomatic relief for pain and inflammation in both osteoarthritis and rheumatoid arthritis but does not alter the disease course in either condition.

Question 373: What is the mechanism of action of colchicine in acute gout?

A. Renal disease involving interstitial tissues
B. Uric acid nephrolithiasis
C. Deficiency of enzyme Xanthine oxidase
D. Inhibition of leukocyte migration and phagocytosis (Correct Answer)

Explanation: ***Inhibition of leukocyte migration and phagocytosis*** - Colchicine primarily exerts its anti-inflammatory effect in acute gout by **binding to tubulin**, which inhibits microtubule polymerization. - This action disrupts essential cellular functions in inflammatory cells, particularly **neutrophils**, thereby reducing their migration to inflamed sites and their ability to phagocytose uric acid crystals. *Renal disease involving interstitial tissues* - This option describes a potential complication or manifestation of gout, such as **urate nephropathy**, rather than the mechanism of action of colchicine. - Colchicine does not directly target or treat pre-existing renal interstitial tissue disease as its primary mechanism for acute gout relief. *Uric acid nephrolithiasis* - This condition involves the formation of **kidney stones from uric acid** and is a consequence of chronic hyperuricemia. - Colchicine is not used to acutely treat or prevent the formation of uric acid kidney stones; its role is in managing the inflammatory arthritis of gout. *Deficiency of enzyme Xanthine oxidase* - **Xanthine oxidase** is an enzyme involved in the production of uric acid, and its inhibition (e.g., by allopurinol or febuxostat) is a strategy to lower uric acid levels in the blood. - Colchicine does not affect xanthine oxidase activity; it works downstream by modulating the inflammatory response to uric acid crystals.

Question 374: All of the following are effective topically except-

A. Amethocaine
B. Procaine (Correct Answer)
C. Lidocaine
D. Cocaine

Explanation: ***Procaine*** - **Procaine** is an ester-type local anesthetic with poor topical penetration due to its **chemical structure and low lipophilicity**. - It is primarily used for **infiltration anesthesia** and nerve blocks, requiring direct injection into tissues to achieve its local anesthetic effects. *Amethocaine* - **Amethocaine** (tetracaine) is a potent ester local anesthetic that is very effective for **topical anesthesia**, particularly on mucous membranes and the eye. - Its high lipophilicity allows for good absorption through the skin and mucous membranes, providing prolonged anesthetic effects. *Lidocaine* - **Lidocaine** is an amide-type local anesthetic that is widely used for **topical anesthesia** due to its excellent penetration and rapid onset of action. - It is available in various forms such as creams, gels, and patches for surface anesthesia. *Cocaine* - **Cocaine** is a naturally occurring ester local anesthetic that is highly effective topically, particularly on **mucous membranes** (e.g., nasal passages). - Besides its local anesthetic properties, it also causes **vasoconstriction**, which helps to reduce bleeding.

Question 375: Tocilizumab used against rheumatoid arthritis is a monoclonal antibody against:

A. Interleukin-5 receptor
B. Interleukin-5
C. Interleukin-6
D. Interleukin-6 receptor (Correct Answer)

Explanation: ***Interleukin-6 receptor*** - **Tocilizumab** is a recombinant **humanized monoclonal antibody** that targets and blocks the **interleukin-6 (IL-6) receptor**. - By blocking the IL-6 receptor, tocilizumab inhibits the signaling of IL-6, a **pro-inflammatory cytokine** implicated in the pathogenesis of **rheumatoid arthritis (RA)** and other autoimmune diseases. *Interleukin-5 receptor* - Monoclonal antibodies targeting the **interleukin-5 receptor (IL-5R)**, such as **benralizumab**, are used primarily for **severe asthma with an eosinophilic phenotype**, not rheumatoid arthritis. - Blocking IL-5R reduces the production and survival of **eosinophils**, which are key effector cells in allergic inflammation. *Interleukin-5* - Antibodies against **interleukin-5 (IL-5)**, like **mepolizumab** and **reslizumab**, are also indicated for **severe eosinophilic asthma**. - IL-5 directly promotes the growth, differentiation, and activation of **eosinophils**, a mechanism distinct from rheumatoid arthritis pathogenesis. *Interleukin-6* - While **interleukin-6 (IL-6)** is a pro-inflammatory cytokine, tocilizumab directly targets its **receptor**, not the cytokine itself. - Other biologics might target the cytokine directly, but tocilizumab's mechanism involves **receptor blockade** to prevent IL-6 binding and signaling.

Question 376: Drug X is useful in the treatment of rheumatoid arthritis. It is available only in the parenteral formulation and its mechanism of action is antagonism of tumor necrosis factor. Which of the following can be X?

A. Cyclosporine
B. Etanercept (Correct Answer)
C. Phenylbutazone
D. Penicillamine

Explanation: ***Etanercept*** - **Etanercept** is a **tumor necrosis factor (TNF)-alpha inhibitor** used in the treatment of **rheumatoid arthritis** [1], and it is administered via **subcutaneous injection** (parenteral) [1]. - Its mechanism of action involves binding to and **inactivating TNF-alpha**, a key cytokine in the inflammatory process of rheumatoid arthritis [1].*Cyclosporine* - **Cyclosporine** is an **immunosuppressant** that primarily acts by inhibiting **calcineurin**, thereby reducing T-lymphocyte activity, not directly antagonizing TNF. - While used in some autoimmune conditions, it is available in **oral and intravenous formulations** and is not primarily identified as a TNF antagonist.*Phenylbutazone* - **Phenylbutazone** is a **nonsteroidal anti-inflammatory drug (NSAID)** that inhibits **prostaglandin synthesis**, providing symptomatic relief from pain and inflammation. - It does not target TNF and is associated with significant **adverse effects**, leading to its limited use in modern medicine.*Penicillamine* - **Penicillamine** is a **disease-modifying antirheumatic drug (DMARD)** with a mechanism of action that is not fully understood, but it is thought to reduce immune complex formation and suppress T-cell activity. - It is an **oral medication** and its primary action is not TNF antagonism; its use has largely been replaced by newer, more effective DMARDs.

Question 377: Which drug used in treatment of rheumatoid arthritis acts by inhibition of T-cell proliferation?

A. Anakinra
B. Leflunomide (Correct Answer)
C. Infliximab
D. Etanercept

Explanation: ***Leflunomide*** - **Leflunomide** is a **pyrimidine synthesis inhibitor** that works by inhibiting the enzyme **dihydroorotate dehydrogenase** [1]. - This inhibition leads to a decrease in **de novo pyrimidine synthesis**, which is essential for **T-cell proliferation**, thereby exerting its immunomodulatory effects in **rheumatoid arthritis** [1], [2]. *Anakinra* - **Anakinra** is an **interleukin-1 receptor antagonist** that blocks the activity of **IL-1**, a pro-inflammatory cytokine. - It does not primarily act by inhibiting **T-cell proliferation**, but rather by modulating the inflammatory response. *Infliximab* - **Infliximab** is a **monoclonal antibody** that targets and neutralizes **tumor necrosis factor-alpha (TNF-α)**, a key cytokine in inflammation. - Its mechanism of action is primarily related to blocking **TNF-α activity**, not directly inhibiting **T-cell proliferation**. *Etanercept* - **Etanercept** is a **fusion protein** that acts as a **TNF-α receptor decoy**, binding to **TNF-α** and preventing it from interacting with its natural receptors. - Similar to infliximab, its main action is to inhibit **TNF-α**, rather than directly inhibiting **T-cell proliferation**.

Question 378: A 50-year-old man presents with complaints of bilateral morning stiffness in his wrists and knees and painful joints on exercise. On physical examination, the joints are slightly swollen. The rest of the examination is unremarkable. His laboratory findings are also negative except for slight anemia, elevated erythrocyte sedimentation rate, and positive rheumatoid factor. The patient was started on weekly methotrexate to control the inflammation. What is the principle mechanism of action here?

A. Inhibition of assembly of microtubules in neutrophils impairing chemotaxis
B. Increased extracellular levels of adenosine (Correct Answer)
C. Inhibition of cyclooxygenase enzyme
D. Inhibition of Dihydrofolate reductase enzyme

Explanation: ***Increased extracellular levels of adenosine*** - Methotrexate, at the low doses used for rheumatoid arthritis, primarily acts by inhibiting **aminoimidazole carboxamide ribonucleotide (AICAR) transformylase**, leading to a buildup of AICAR. - This accumulation inhibits **adenosine deaminase** and **AMP deaminase**, increasing extracellular adenosine, which is an anti-inflammatory mediator. *Inhibition of assembly of microtubules in neutrophils impairing chemotaxis* - This mechanism is characteristic of **colchicine**, used in treating gout, not methotrexate in rheumatoid arthritis. - Colchicine prevents neutrophil migration and activity by disrupting **microtubule polymerization**. *Inhibition of cyclooxygenase enzyme* - This is the primary mechanism of action for **NSAIDs (Nonsteroidal Anti-inflammatory Drugs)**, which reduce inflammation and pain by blocking prostaglandin synthesis. - Methotrexate's anti-inflammatory effects are not mediated through direct cyclooxygenase inhibition. *Inhibition of Dihydrofolate reductase enzyme* - While methotrexate does inhibit **dihydrofolate reductase (DHFR)**, this mechanism is primarily responsible for its cytotoxic effects in **cancer chemotherapy** at much higher doses. - At the low doses used in rheumatoid arthritis, the primary anti-inflammatory mechanism is related to adenosine.

Question 379: All are opioid agonist - antagonist compounds except

A. Pentazocine
B. Buprenorphine
C. Nalbuphine
D. Nalmefene (Correct Answer)

Explanation: ***Nalmefene*** - **Nalmefene** is a **pure opioid antagonist**, meaning it blocks opioid receptors without producing any opioid agonist effects [1], [4]. - It is primarily used to reverse opioid overdose and for alcohol dependence treatment. - Unlike agonist-antagonist compounds, it has **no agonist activity** at any opioid receptor, making it the correct answer [1], [4]. *Pentazocine* - **Pentazocine** is a classic **opioid agonist-antagonist** (mixed agonist-antagonist). - It acts as an **agonist at kappa receptors** (providing analgesia) and a **weak antagonist or partial agonist at mu receptors** [2]. - This mixed action produces a ceiling effect on respiratory depression and lower abuse potential compared to pure mu agonists [2]. *Buprenorphine* - **Buprenorphine** is a **partial mu opioid agonist** with high receptor affinity and antagonist activity at kappa receptors [2]. - While sometimes grouped with agonist-antagonists due to its mixed receptor activity, it's more accurately classified as a **partial agonist** [2]. - Its partial agonist activity at mu receptors provides effective analgesia with a ceiling effect on respiratory depression, making it useful for pain management and opioid dependence treatment [3]. *Nalbuphine* - **Nalbuphine** is a classic **opioid agonist-antagonist** compound [2]. - It acts as an **agonist at kappa receptors** and an **antagonist at mu receptors** [2]. - Provides analgesia similar to morphine but with a ceiling effect on respiratory depression and lower dependence potential [2].

Question 380: Morphine should not be used in the treatment of:

A. Cancer pain
B. Ischemic pain
C. Biliary colic (Correct Answer)
D. Postoperative pain

Explanation: ***Biliary colic*** - Morphine can cause **spasms of the sphincter of Oddi**, leading to an increase in biliary pressure and potentially exacerbating the pain of biliary colic. - This adverse effect can worsen the patient's condition rather than alleviate it, making alternative analgesics like **pethidine (meperidine)** or **NSAIDs** more appropriate for biliary pain. *Cancer pain* - Morphine is a **first-line opioid** for managing moderate to severe cancer pain, providing effective analgesia as part of a comprehensive pain management strategy. - Its efficacy in cancer pain is well-established, and doses can be titrated to achieve optimal pain control without significant risk of addiction in this context. *Postoperative pain* - Morphine is widely used for **postoperative pain management** due to its potent analgesic effects and predictable pharmacokinetics. - It is effective in reducing acute surgical pain and can be administered via various routes, including intravenous and epidural, to suit patient needs. *Ischemic pain* - Morphine is effective in treating ischemic pain, particularly in conditions like **myocardial infarction**, where it helps to reduce pain, anxiety, and **myocardial oxygen demand**. - While it was favored historically because of its action as a **venodilator** and **anxiolytic**, it is now used with caution in acute coronary syndromes, specifically because it can delay the absorption of oral antiplatelet drugs.

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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