NSAIDs: Classification and Mechanism — MCQs
What is the mechanism of action of ticagrelor?
Which of the following drugs is useful in acute attack of gout ?
Anti-inflammatory action of steroids is due to
Which enzyme is primarily inhibited by the drug prednisolone, leading to its anti-inflammatory effects?
Mechanism of action of aspirin in pain relief is:
Which of the following is a false statement?
Which of the following is the most appropriate pharmacological treatment for neuropathic pain in a diabetic patient?
Which drug is commonly used for outpatient department (OPD) analgesia?
Pegloticase is used for the treatment of:
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?
NSAIDs: Classification and Mechanism Indian Medical PG Practice Questions and MCQs
Question 1: What is the mechanism of action of ticagrelor?
- A. PAR1 activator
- B. P2Y12 inhibitor (Correct Answer)
- C. P2Y12 activator
- D. PAR1 inhibitor
Explanation: ***P2Y12 inhibitor*** - Ticagrelor is an **oral antiplatelet agent** that works by reversibly binding to the **P2Y12 receptor** on platelets. - This binding prevents adenosine diphosphate (ADP) from activating the P2Y12 receptor, which is crucial for **platelet aggregation** and **thrombus formation**. *PAR1 inhibitor* - **PAR1 inhibitors** (e.g., vorapaxar) block the thrombin receptor on platelets, leading to antiplatelet effects. - This mechanism is distinct from ticagrelor's action on the P2Y12 receptor. *PAR1 activator* - Activating **PAR1** would promote platelet aggregation and activation, which is the opposite effect of an antiplatelet medication like ticagrelor. - This mechanism would increase the risk of thrombosis. *P2Y12 activator* - Activating the **P2Y12 receptor** would lead to increased platelet aggregation and is not the mechanism of action for an antiplatelet drug. - Drugs that activate P2Y12 would promote the formation of blood clots.
Question 2: Which of the following drugs is useful in acute attack of gout ?
- A. Furosemide
- B. Sulfinpyrazone
- C. Allopurinol
- D. Piroxicam (Correct Answer)
Explanation: ***Piroxicam*** - **Piroxicam** is a **non-steroidal anti-inflammatory drug (NSAID)**, which are the first-line treatment for acute gout attacks. - NSAIDs work by inhibiting **prostaglandin synthesis**, thereby reducing inflammation and pain associated with the acute crystal-induced arthritis. *Furosemide* - **Furosemide** is a loop diuretic that can **raise uric acid levels** by increasing reabsorption in the renal tubules. - Therefore, it would exacerbate **gout** and is contraindicated during an acute attack. *Sulfinpyrazone* - **Sulfinpyrazone** is a **uricosuric agent** used for chronic gout management to increase uric acid excretion. - It is **not used for acute attacks** as it can precipitate or worsen an attack by mobilizing uric acid crystals. *Allopurinol* - **Allopurinol** is a **xanthine oxidase inhibitor** used for long-term management of hyperuricemia and chronic gout. - Starting allopurinol during an **acute attack** can worsen or prolong the attack by causing rapid changes in serum uric acid levels.
Question 3: Anti-inflammatory action of steroids is due to
- A. Inhibition of lipoxygenase
- B. Inhibition of phospholipase A2 (Correct Answer)
- C. Inhibition of cyclooxygenase
- D. Increased activity of lipoprotein lipase
Explanation: ***Inhibition of phospholipase A2*** - Steroids exert their potent anti-inflammatory effects primarily by inducing the synthesis of **lipocortin-1 (annexin-1)**, which then inhibits **phospholipase A2 (PLA2)** activity. - This inhibition of PLA2 prevents the release of **arachidonic acid** from cell membrane phospholipids, thereby blocking the entire cascade of downstream inflammatory mediators, including prostaglandins, thromboxanes, and leukotrienes. *Inhibition of lipoxygenase* - While leukotrienes (products of the lipoxygenase pathway) are inflammatory mediators, steroids achieve their effect upstream by blocking the precursor (arachidonic acid) rather than directly inhibiting **lipoxygenase**. - **Zileuton** is an example of a drug that directly inhibits lipoxygenase. *Inhibition of cyclooxygenase* - Steroids do not directly inhibit **cyclooxygenase (COX) enzymes**; this is the primary mechanism of action for **NSAIDs (Nonsteroidal Anti-inflammatory Drugs)** like ibuprofen and aspirin. - By inhibiting COX, NSAIDs primarily block the synthesis of prostaglandins and thromboxanes, but not leukotrienes. *Increased activity of lipoprotein lipase* - Increased activity of **lipoprotein lipase (LPL)** by steroids is related to their metabolic effects, such as promoting fat deposition and contributing to steroid-induced dyslipidemia, rather than their anti-inflammatory action. - LPL's role is in the metabolism of triglycerides in lipoproteins, which is distinct from the inflammatory cascade.
Question 4: Which enzyme is primarily inhibited by the drug prednisolone, leading to its anti-inflammatory effects?
- A. Lipoxygenase
- B. Phosphodiesterase
- C. Phospholipase A2 (Correct Answer)
- D. Cyclooxygenase
Explanation: ***Phospholipase A2*** - Prednisolone, a corticosteroid, primarily exerts its anti-inflammatory effects by inhibiting **phospholipase A2**. - Inhibition of **phospholipase A2** prevents the release of **arachidonic acid** from cell membrane phospholipids, thereby blocking the synthesis of all downstream inflammatory mediators. *Cyclo oxygenase* - **Cyclooxygenase (COX)** enzymes are responsible for converting arachidonic acid into **prostaglandins, prostacyclins**, and **thromboxanes**. - While COX is involved in inflammation, it is primarily inhibited by **NSAIDs**, not directly by prednisolone as its initial target. *Lipoxygenase* - **Lipoxygenase (LOX)** enzymes metabolize arachidonic acid into **leukotrienes**, other potent inflammatory mediators. - While leukotrienes contribute to inflammation, prednisolone's primary mechanism of action is upstream of both COX and LOX pathways, rather than direct LOX inhibition. *Phosphodiesterase* - **Phosphodiesterases (PDEs)** are a diverse group of enzymes that break down cyclic nucleotides (cAMP and cGMP). - PDE inhibitors are used for conditions like asthma and erectile dysfunction, and their inhibition is not the primary mechanism of action for the anti-inflammatory effects of prednisolone.
Question 5: Mechanism of action of aspirin in pain relief is:
- A. Enhances opioid action
- B. Activates serotonin receptors
- C. Inhibits COX enzymes (Correct Answer)
- D. Blocks NMDA receptors
Explanation: **Inhibits COX enzymes** - **Aspirin** exerts its analgesic effects primarily by **irreversibly inhibiting** cyclooxygenase (COX) enzymes, particularly COX-1 and COX-2. - This inhibition reduces the synthesis of **prostaglandins**, which are important mediators of pain and inflammation. *Enhances opioid action* - Opioids primarily act on **opioid receptors** in the central nervous system to reduce pain perception. - Aspirin does not directly enhance opioid action; while they can be used together for additive pain relief, their mechanisms are distinct. *Activates serotonin receptors* - Activation of **serotonin receptors** (5-HT receptors) can play a role in pain modulation, but aspirin's primary mechanism is not through these receptors. - Some antidepressants and triptans exert their effects via serotonin receptors. *Blocks NMDA receptors* - **NMDA receptors** are involved in neuronal excitability and the processing of pain signals, particularly in chronic pain. - Drugs that block NMDA receptors, such as ketamine, have analgesic properties but this is not the mechanism of action for aspirin.
Question 6: Which of the following is a false statement?
- A. Acetaminophen does not have anti-inflammatory action
- B. Non-selective COX inhibitors are contraindicated in postoperative patients
- C. NSAID with least cardiovascular risk is Naproxen
- D. Gastric irritation is more severe with NSAIDs compared to aspirin (Correct Answer)
Explanation: ***Gastric irritation is more severe with NSAIDs compared to aspirin*** - This statement is **FALSE** and is the correct answer to this question. - Aspirin, even at low doses, has a **higher propensity** for causing gastric irritation and bleeding than many other NSAIDs. - Aspirin causes direct mucosal injury and irreversibly inhibits COX-1, leading to prolonged **antiplatelet effects** and increased GI bleeding risk. - Most non-aspirin NSAIDs cause less severe gastric irritation in comparison. *Non-selective COX inhibitors are contraindicated in postoperative patients* - This statement is **not entirely accurate** but not the best answer. - Non-selective NSAIDs are commonly used in **multimodal postoperative analgesia**. - While they require caution due to **bleeding risk**, **renal dysfunction**, and **cardiovascular events**, they are not absolutely contraindicated. - They are often used with appropriate patient selection and monitoring. *Acetaminophen does not have anti-inflammatory action* - This statement is **TRUE**. - Acetaminophen (paracetamol) acts primarily as an **analgesic** and **antipyretic** through central COX inhibition. - It lacks significant peripheral anti-inflammatory effects, distinguishing it from NSAIDs. *NSAID with least cardiovascular risk is Naproxen* - This statement is **TRUE**. - Among traditional NSAIDs, **naproxen** is associated with the lowest cardiovascular risk. - It does not significantly increase the risk of thrombotic events like **myocardial infarction** or stroke compared to other NSAIDs.
Question 7: Which of the following is the most appropriate pharmacological treatment for neuropathic pain in a diabetic patient?
- A. Acetaminophen
- B. Tramadol
- C. Aspirin
- D. Gabapentin (Correct Answer)
Explanation: ***Gabapentin*** - **Gabapentin** is a widely recommended first-line treatment for diabetic neuropathic pain due to its efficacy in modulating neuronal excitability. - It works by binding to the **α2δ subunit of voltage-gated calcium channels**, reducing calcium influx and thereby decreasing the release of excitatory neurotransmitters involved in pain signaling. *Acetaminophen* - **Acetaminophen** is primarily an analgesic and antipyretic, effective for mild to moderate non-neuropathic pain. - It has no significant efficacy against **neuropathic pain**, which involves distinct neurobiological mechanisms. *Tramadol* - **Tramadol** is an opioid analgesic with some serotonin and norepinephrine reuptake inhibition, offering moderate pain relief. - While it can be used for moderate to severe pain, it is generally considered a **second-line agent** for neuropathic pain due to its opioid nature and potential side effects. *Aspirin* - **Aspirin** is a nonsteroidal anti-inflammatory drug (NSAID) primarily used for its anti-inflammatory, analgesic, and antiplatelet effects. - It is **ineffective for neuropathic pain**, which does not typically involve peripheral inflammation as its primary mechanism.
Question 8: Which drug is commonly used for outpatient department (OPD) analgesia?
- A. Diclofenac
- B. Ibuprofen
- C. Paracetamol (Correct Answer)
- D. Tramadol
Explanation: ***Paracetamol*** - It is a widely used and generally **safe analgesic** and antipyretic often prescribed for mild to moderate pain in an outpatient setting. - Its favorable side effect profile and availability as an **over-the-counter (OTC)** medication make it a first-choice drug for many common pain conditions. *Diclofenac* - While it is an effective NSAID used for pain and inflammation, its use can be associated with **gastrointestinal side effects** like ulcers and bleeding, as well as cardiovascular risks. - It is often reserved for more significant inflammatory pain or when other analgesics are insufficient, and may require more careful monitoring in an outpatient setting. *Ibuprofen* - Similar to diclofenac, Ibuprofen is an **NSAID** which is effective for pain and inflammation. However, it also carries risks of **gastrointestinal irritation** and renal side effects, especially with prolonged use or in certain patient populations. - While available OTC, its use for routine outpatient analgesia may be less preferred than paracetamol in some cases due to its GI and renal side effect profile. *Tramadol* - Tramadol is a **central acting opioid analgesic** with a higher potential for side effects such as nausea, dizziness, constipation, and the risk of dependence or abuse. - It is typically reserved for moderate to severe pain that is not adequately managed by non-opioid analgesics, and its prescription often involves more stringent monitoring than paracetamol.
Question 9: Pegloticase is used for the treatment of:
- A. CPPD
- B. Chronic tophaceous gout (Correct Answer)
- C. Refractory Rheumatoid Arthritis
- D. Reactive Arthritis
Explanation: ### Chronic tophaceous gout - **Pegloticase** is a recombinant mammalian **uricase** enzyme that converts uric acid to allantoin, which is readily excreted, making it highly effective for lowering **serum uric acid** levels [1]. - It is specifically indicated for the treatment of **chronic refractory gout**, particularly in patients with **tophi** that have not responded to conventional therapies. *CPPD* - **Calcium pyrophosphate dihydrate (CPPD) crystal deposition disease**, also known as pseudogout, is characterized by the deposition of **calcium pyrophosphate crystals** in joints. - Treatment for CPPD primarily involves **NSAIDs**, **colchicine**, or **corticosteroids** for acute attacks, and there is no role for uric acid-lowering agents like pegloticase. *Refractory Rheumatoid Arthritis* - **Rheumatoid arthritis (RA)** is an autoimmune disease characterized by chronic inflammation of the joints, and its treatment focuses on **disease-modifying antirheumatic drugs (DMARDs)**, biologics (e.g., TNF inhibitors, rituximab), and JAK inhibitors [2]. - Pegloticase is a uricase and is not indicated for the treatment of RA, as RA pathogenesis does not involve **uric acid metabolism**. *Reactive Arthritis* - **Reactive arthritis** is a seronegative spondyloarthropathy that typically develops after a **genitourinary** or **gastrointestinal infection**. - Its management involves treating the underlying infection (if ongoing), **NSAIDs**, intra-articular **corticosteroids**, and sometimes **DMARDs**, none of which include uric acid-lowering agents.
Question 10: 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.
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