Analgesics and Anti-inflammatory Drugs — MCQs

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

Question 381: A patient presented with pain in the right lower quadrant of abdomen. He has history of renal stones in right kidney. He was prescribed an opioid which is agonist at kappa receptors and antagonist at mu receptors. The likely drug given was:

A. Pentazocine (Correct Answer)
B. Tramadol
C. Buprenorphine
D. Fentanyl

Explanation: ***Pentazocine*** - **Pentazocine** is a **mixed agonist-antagonist opioid analgesic** that acts as an **agonist at kappa opioid receptors** and a **weak antagonist or partial agonist at mu opioid receptors**. - This unique receptor profile makes it the drug described in the question. - It is effective for **moderate to severe pain** including **renal colic** (pain from renal stones), while having a **lower abuse potential** and **ceiling effect on respiratory depression** compared to pure mu agonists. *Tramadol* - **Tramadol** is a synthetic opioid that acts primarily as a **weak mu-opioid receptor agonist** and also inhibits the reuptake of **norepinephrine** and **serotonin**. - It does **not** have significant kappa receptor agonism or mu receptor antagonism. - Does not fit the description given in the question. *Buprenorphine* - **Buprenorphine** is a **partial agonist at mu opioid receptors** and an **antagonist at kappa opioid receptors**. - This receptor activity profile is the **opposite** of what is described in the question (which asks for kappa agonist, mu antagonist). *Fentanyl* - **Fentanyl** is a highly potent **pure mu-opioid receptor agonist**. - It has **no significant kappa receptor agonism** or mu receptor antagonism. - Does not match the pharmacological profile described in the question.

Question 382: 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 383: Pegloticase is used in:

A. Rheumatoid arthritis
B. Paralytic ileus
C. Chronic gout (Correct Answer)
D. Psoriatic arthritis

Explanation: ***Chronic gout*** - Pegloticase is an enzyme that converts **uric acid to allantoin**, a more water-soluble compound readily excreted by the kidneys. - It is specifically approved for the treatment of **chronic, refractory gout** in patients who have failed to achieve target serum uric acid levels with conventional therapies. *Rheumatoid arthritis* - This condition is an **autoimmune inflammatory disease** primarily affecting the joints. - Treatment typically involves **DMARDs** (disease-modifying antirheumatic drugs) such as methotrexate, biologics, and corticosteroids, not pegloticase. *Paralytic ileus* - This is a condition characterized by the **absence of bowel motility**, often due to surgery, medications, or electrolyte imbalances. - Management focuses on supportive care, addressing the underlying cause, and sometimes prokinetic agents, but not pegloticase. *Psoriatic arthritis* - This is a specific type of **inflammatory arthritis** associated with psoriasis. - Treatment regimens for psoriatic arthritis usually involve DMARDs, biologics (like TNF inhibitors), and NSAIDs, rather than pegloticase.

Question 384: 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 385: 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 386: Which of the following pain medications requires the MOST caution in a patient with a history of opioid addiction?

A. Morphine (Correct Answer)
B. Oxycodone
C. Methadone
D. Buprenorphine

Explanation: ***Morphine*** - Morphine is a **full mu-opioid agonist** with the highest potential for **abuse, dependence, and relapse** in patients with a history of opioid addiction due to its strong **euphoric effects**. - It carries the greatest risk of triggering **addictive behaviors** and relapse in recovering patients, making it require the MOST caution in this population. - Use should be avoided if possible, or limited to short-term use under strict supervision with alternative analgesics preferred. *Oxycodone* - Oxycodone is another **potent full opioid agonist** with very high abuse potential, nearly equivalent to morphine. - While requiring extreme caution, morphine remains the prototypical high-risk opioid in addiction-prone patients. *Methadone* - Methadone is a **long-acting full opioid agonist** used in opioid maintenance therapy with significant abuse potential. - However, when used appropriately in supervised programs, it has a role in addiction treatment, though acute pain prescribing requires caution due to its **long half-life and QTc prolongation risk**. *Buprenorphine* - Buprenorphine is a **partial mu-opioid agonist** with a **ceiling effect** that limits respiratory depression and euphoria. - It is the **standard medication for opioid use disorder treatment** and has LOWER abuse potential than full agonists. - While it requires careful timing to avoid precipitated withdrawal in opioid-dependent patients, it is actually SAFER than full agonists in patients with addiction history due to reduced relapse risk.

Question 387: Which of the following is an absolute contraindication to the use of nonsteroidal anti-inflammatory drugs (NSAIDs)?

A. Asthma
B. Rheumatoid arthritis
C. Hypertension
D. Active peptic ulcer disease (Correct Answer)

Explanation: ***Active peptic ulcer disease*** - NSAIDs **inhibit cyclooxygenase (COX)** enzymes, which are responsible for producing **prostaglandins** that protect the gastric mucosa. - In patients with **active peptic ulcers**, this inhibition can lead to serious complications like **bleeding** or **perforation**, making it an **absolute contraindication**. - A history of peptic ulcer disease is a relative contraindication, but active disease is an absolute contraindication. *Asthma* - While NSAIDs can exacerbate asthma in susceptible individuals (**NSAID-exacerbated respiratory disease or aspirin-exacerbated respiratory disease**), it is usually a **relative contraindication** rather than an absolute one. - This reaction typically affects a specific subset of asthmatic patients (around 10-20%) with aspirin sensitivity and nasal polyps. *Rheumatoid arthritis* - NSAIDs are commonly used to **manage pain and inflammation** associated with rheumatoid arthritis. - It is a condition where NSAIDs are **indicated** for symptom relief, not a contraindication. *Hypertension* - NSAIDs can contribute to **elevated blood pressure** due to their effects on renal prostaglandin synthesis, leading to sodium and water retention. - Although NSAIDs should be used cautiously in hypertensive patients, it is considered a **relative contraindication**, requiring close monitoring rather than an absolute prohibition.

Question 388: How do antipyretic medications help in reducing fever?

A. They reduce sweating
B. They constrict blood vessels
C. They directly cool the body
D. They inhibit prostaglandin synthesis (Correct Answer)

Explanation: ***They inhibit prostaglandin synthesis.*** - Fever is mediated by **prostaglandins**, specifically **PGE2**, which are released in response to pyrogens and act on the **hypothalamus** to raise the body's set point. - Antipyretics like **NSAIDs** (e.g., ibuprofen, aspirin) and **acetaminophen** (paracetamol) primarily work by inhibiting the enzyme **cyclooxygenase (COX)**, thereby reducing the production of these fever-inducing prostaglandins. *They reduce sweating* - Reducing sweating would impair the body's natural cooling mechanism and **exacerbate fever**, not reduce it. - Sweating is a **thermoregulatory response** to actively cool the body when its temperature set point is lowered. *They constrict blood vessels* - **Vasoconstriction** reduces heat loss from the skin and is a process the body uses **to conserve heat** or **raise body temperature**, which would worsen fever. - Antipyretics promote **vasodilation** as part of the body's heat loss mechanisms once the hypothalamic set point is reset. *They directly cool the body* - Antipyretics act **pharmacologically** to modulate internal physiological processes, not by physically or directly cooling the body. - Direct cooling methods like cold compresses or sponging are **external interventions**, distinct from the action of antipyretic medications.

Question 389: A patient with an autoimmune disease is prescribed an anti-inflammatory drug that inhibits phospholipase A2. Which drug is appropriate?

A. Methotrexate
B. Aspirin
C. Celecoxib
D. Prednisone (Correct Answer)

Explanation: ***Prednisone*** - **Corticosteroids** like prednisone mimic natural glucocorticoids and are potent **anti-inflammatory** agents. - They inhibit **phospholipase A2**, thereby preventing the release of **arachidonic acid** from cell membranes, which is the precursor for prostaglandins and leukotrienes. *Methotrexate* - This is a **disease-modifying antirheumatic drug (DMARD)** primarily used as an **immunosuppressant** in autoimmune diseases. - Its mechanism involves inhibiting **dihydrofolate reductase**, which interferes with DNA synthesis, but it does not directly inhibit **phospholipase A2**. *Aspirin* - **Aspirin** is a **non-steroidal anti-inflammatory drug (NSAID)** that works by irreversibly inhibiting **cyclooxygenase (COX) enzymes 1 and 2**. - It does not inhibit **phospholipase A2**, but rather acts downstream in the arachidonic acid pathway. *Celecoxib* - **Celecoxib** is a **selective COX-2 inhibitor**, belonging to the NSAID class. - It specifically targets **COX-2** to reduce inflammation with fewer gastrointestinal side effects compared to non-selective NSAIDs, but it does not inhibit **phospholipase A2**.

Question 390: A patient presents with an acute gout attack. Which medication is contraindicated in the acute setting due to the risk of exacerbating the attack?

A. Colchicine
B. Indomethacin
C. Allopurinol (Correct Answer)
D. Prednisone

Explanation: ***Allopurinol*** - Initiating or increasing the dose of **allopurinol** during an acute gout attack can precipitate or worsen the attack. - Allopurinol is a **urate-lowering therapy** that mobilizes uric acid from tissues, potentially leading to a transient increase in serum uric acid during initiation. *Colchicine* - **Colchicine** is a first-line treatment for acute gout attacks, especially when started within 24-36 hours of symptom onset. - It works by inhibiting neutrophil migration and activation, reducing the inflammatory response to uric acid crystals. *Indomethacin* - **Indomethacin** is a non-steroidal anti-inflammatory drug (NSAID) commonly used to treat the acute pain and inflammation of a gout attack. - It rapidly reduces inflammation by inhibiting prostaglandin synthesis, providing symptomatic relief. *Prednisone* - **Prednisone**, a corticosteroid, is effective in treating acute gout attacks, particularly when NSAIDs or colchicine are contraindicated or ineffective. - It powerfully suppresses the inflammatory response, quickly resolving the pain and swelling associated with gout flares.

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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