Analgesics and Anti-inflammatory Drugs — MCQs

An otherwise healthy 15-month-old boy is brought to the emergency department by his mother 1 hour after having a single episode of generalized tonic-clonic seizure, which stopped spontaneously after 1 minute. He was sleepy initially but is now awake and alert. His mother reports that he has had a fever and runny nose for the past 3 days. His temperature is 40.1°C (104.2°F). Physical examination shows no abnormalities. Analysis of his cerebrospinal fluid shows 3 cells/mm3, a glucose concentration of 68 mg/dL, and a protein concentration of 35 mg/dL. Administration of a drug that acts through which of the following mechanisms of action is most appropriate in this patient?

Q368

Shortest acting local anaesthetic

Q369

Drug used in osteoarthritis

Q370

NSAID used commonly for topical ocular use is

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

Question 361: A female patient complains of swelling and pain in her great toe. Her uric acid level is found to be high. A drug that reduces uric acid levels is prescribed. Which of the following enzymes should the drug inhibit?

A. Lysyl oxidase
B. Xanthine oxidase (Correct Answer)
C. Homogentisate oxidase
D. Urease

Explanation: ***Xanthine oxidase*** - **Xanthine oxidase** catalyzes the conversion of hypoxanthine to xanthine and xanthine to uric acid in the purine degradation pathway - **Xanthine oxidase inhibitors** (allopurinol, febuxostat) are the mainstay drugs for chronic management of hyperuricemia and gout - By inhibiting this enzyme, these drugs reduce uric acid production, lowering serum uric acid levels and preventing crystal deposition in joints - The clinical presentation of **podagra** (acute pain and swelling of the great toe) with elevated uric acid is classic for **acute gouty arthritis** *Lysyl oxidase* - Involved in cross-linking collagen and elastin in connective tissue formation - Not related to purine metabolism or uric acid synthesis - Inhibition would affect collagen strength, not uric acid levels *Homogentisate oxidase* - Enzyme in the tyrosine degradation pathway - Deficiency causes alkaptonuria (accumulation of homogentisic acid) - Not involved in purine metabolism *Urease* - Bacterial enzyme that hydrolyzes urea to ammonia and carbon dioxide - Found in bacteria like *Helicobacter pylori* and *Proteus* species - Not involved in human uric acid synthesis or metabolism

Question 362: A 60 -year-old patient of carcinoma prostate is having skeletal metastasis. He was put on 8 mg of hydromorphone daily but is still having severe bone pain. He was then put on the transdermal system shown below. All are correct about this transdermal system except:

A. Exposure to heat can result in overdose
B. Respiratory depression is a chief hazard
C. Put the new patch at the same site to prevent skin sensitization (Correct Answer)
D. Abuse liability similar to opioids

Explanation: ***Put the new patch at the same site to prevent skin sensitization*** - It is recommended to **rotate application sites** for transdermal patches (like fentanyl patches) to prevent **skin irritation**, sensitization, and potential local reactions. - Applying a new patch to the same site can lead to **incomplete absorption** and localized skin issues, compromising drug delivery and comfort. *Exposure to heat can result in overdose* - **Heat increases the rate of drug absorption** from transdermal fentanyl patches, leading to a potentially fatal overdose. - Patients should be advised to **avoid external heat sources** like heating pads, electric blankets, saunas, and prolonged sun exposure while wearing the patch. *Respiratory depression is a chief hazard* - As a potent opioid, **fentanyl's primary severe adverse effect is respiratory depression**, especially in opioid-naïve patients or with overdose. - This risk is particularly high with transdermal delivery due to its **slow onset and prolonged duration** of action. *Abuse liability similar to opioids* - Fentanyl is a **Schedule II controlled substance** with a **high potential for abuse** and dependence, similar to other potent opioids. - It produces **euphoria and analgesia**, making it a target for misuse, and its potency increases its danger profile in abuse scenarios.

Question 363: Treatment of first choice in acute Gout is

A. Oral Methotrexate
B. Sulfasalazine
C. Allopurinol
D. Oral Colchicine (Correct Answer)

Explanation: ***Oral Colchicine*** - **Colchicine** is highly effective in treating **acute gout attacks** by reducing inflammation caused by uric acid crystal deposition. - It works best when initiated within **24-36 hours** of symptom onset. - Considered a **first-line option** for acute gout, particularly in patients with contraindications to NSAIDs or corticosteroids. - **Mechanism:** Inhibits microtubule polymerization, thereby reducing neutrophil migration and phagocytosis of urate crystals. *Oral Methotrexate* - **Methotrexate** is an **immunosuppressant** primarily used for chronic inflammatory conditions, such as **rheumatoid arthritis** or **psoriasis**. - It is not a first-line treatment for the rapid relief of acute gout symptoms. *Sulfasalazine* - **Sulfasalazine** is an anti-inflammatory and immunomodulatory drug, commonly used in **inflammatory bowel disease** and **rheumatoid arthritis**. - It has no role in the immediate treatment of an acute gout flare. *Allopurinol* - **Allopurinol** is a **xanthine oxidase inhibitor** used for the **long-term prevention** of gout by lowering uric acid levels. - It is generally *not initiated* during an acute attack, as it can potentially worsen the flare by mobilizing urate crystals. - Used for **prophylaxis** in patients with recurrent gout attacks or chronic tophaceous gout.

Question 364: A patient presents with swelling in MCP joints, and his serum uric acid levels were found to be elevated. His physician prescribed a drug which is considered as the first line agent in the management of this condition. What is the mechanism of this drug?

A. Uricosuric drug
B. Pyrimidine antimetabolite
C. Xanthine oxidase inhibitor (Correct Answer)
D. Inhibitor of neutrophil recruitment

Explanation: ***Xanthine oxidase inhibitor*** - The presentation of **swollen MCP joints** and **elevated uric acid** is highly suggestive of **gout**. - **Allopurinol**, a **xanthine oxidase inhibitor**, is the **first-line drug** for chronic gout management, reducing uric acid production. *Uricosuric drug* - **Uricosuric agents** like **probenecid** increase uric acid excretion, but they are generally **second-line** or used in specific cases, not first-line for most patients. - These drugs are typically only effective if there is **sufficient renal function** and are contraindicated in patients with a history of **kidney stones**. *Pyrimidine antimetabolite* - **Pyrimidine antimetabolites** like **5-fluorouracil** are primarily used in **chemotherapy** for certain cancers by interfering with DNA and RNA synthesis. - They have **no role** in the treatment of gout or hyperuricemia. *Inhibitor of neutrophil recruitment* - **Colchicine**, which inhibits neutrophil migration, is used to treat **acute gout flares** by reducing inflammation, but it's not the first-line agent for **long-term management** of hyperuricemia. - This mechanism targets the inflammatory response rather than the underlying **uric acid production** or excretion.

Question 365: What is the mechanism of action of cyclosporine?

A. Inhibition of calcineurin (Correct Answer)
B. Dihydro-orotate dehydrogenase inhibition
C. AMP kinase stimulation
D. IMP dehydrogenase inhibition

Explanation: ***Inhibition of calcineurin*** - Cyclosporine forms a complex with **cyclophilin**, which then inhibits the phosphatase activity of **calcineurin**. - This inhibition prevents the dephosphorylation and subsequent nuclear translocation of **NFAT (nuclear factor of activated T-cells)**, thereby blocking the transcription of **IL-2** and other cytokines essential for T-cell activation. *Dihydro-orotate dehydrogenase inhibition* - This is the mechanism of action of **leflunomide**, another immunosuppressant, which works by inhibiting *de novo* pyrimidine synthesis. - Leflunomide primarily affects rapidly proliferating cells, such as T-lymphocytes, by depriving them of essential pyrimidine nucleotides. *AMP kinase stimulation* - **AMP-activated protein kinase (AMPK)** is a cellular energy sensor that plays a role in metabolism and cellular growth. - While AMPK activation has various cellular effects, it is not the primary mechanism of action for cyclosporine or other calcineurin inhibitors. *IMP dehydrogenase inhibition* - This is the mechanism of action of **mycophenolate mofetil**, an immunosuppressant that selectively inhibits *de novo* guanosine nucleotide synthesis. - By depleting guanosine nucleotides, mycophenolate specifically inhibits the proliferation of T and B lymphocytes.

Question 366: What is the mechanism of action of local anesthetics?

A. Block chloride channels
B. Block calcium channels
C. Block sodium channels (Correct Answer)
D. Block potassium channels

Explanation: ***Block sodium channels*** - Local anesthetics work by **reversibly binding** to the alpha subunit of **voltage-gated sodium channels** on the neuronal membrane. - This binding prevents the influx of sodium ions, thereby inhibiting the **depolarization** of the neuron and **propagation of action potentials**. *Block chloride channels* - **Chloride channels** are primarily involved in **hyperpolarization** or stabilization of the resting membrane potential, and their blockade is not the primary mechanism of local anesthesia. - Drugs like **benzodiazepines** modulate GABA-gated chloride channels for their anxiolytic and sedative effects. *Block calcium channels* - **Calcium channels** are important for neurotransmitter release and muscle contraction, but their blockade is not the way local anesthetics exert their effects. - **Calcium channel blockers** are used in cardiovascular medicine (e.g., diltiazem, verapamil) to reduce heart rate and blood pressure. *Block potassium channels* - **Potassium channels** are crucial for repolarization of the neuronal membrane and maintaining the resting potential. - While some toxins block potassium channels, it is not the principal mechanism by which **local anesthetics** achieve their nerve blocking effect.

Question 367: An otherwise healthy 15-month-old boy is brought to the emergency department by his mother 1 hour after having a single episode of generalized tonic-clonic seizure, which stopped spontaneously after 1 minute. He was sleepy initially but is now awake and alert. His mother reports that he has had a fever and runny nose for the past 3 days. His temperature is 40.1°C (104.2°F). Physical examination shows no abnormalities. Analysis of his cerebrospinal fluid shows 3 cells/mm3, a glucose concentration of 68 mg/dL, and a protein concentration of 35 mg/dL. Administration of a drug that acts through which of the following mechanisms of action is most appropriate in this patient?

A. Blocking voltage-gated Na+ channels
B. Blocking T-type Ca2+ channels
C. Decreasing production of prostaglandin E2 (Correct Answer)
D. Increasing duration of Cl− channel opening

Explanation: Decreasing production of prostaglandin E2 - This patient presents with a **febrile seizure**, characterized by a seizure in the setting of fever without evidence of intracranial infection or metabolic derangement [1]. He has no neurological deficits, and the CSF analysis rules out **meningitis** or **encephalitis**. - The most appropriate treatment for preventing recurrence and managing the fever is an **antipyretic** (e.g., ibuprofen, acetaminophen), which acts by inhibiting **prostaglandin E2** synthesis to reduce the febrile response. *Blocking voltage-gated Na+ channels* - This mechanism is characteristic of several **antiepileptic drugs** (e.g., phenytoin, carbamazepine, lamotrigine), which are typically used for **focal** and **generalized tonic-clonic seizures** [2]. - However, for a simple febrile seizure, chronic antiepileptic therapy is not recommended due to potential side effects and lack of proven benefit in preventing future febrile seizures or epilepsy. *Blocking T-type Ca2+ channels* - This is the primary mechanism of action for **ethosuximide**, an antiepileptic drug specifically used to treat **absence seizures**. - The patient had a generalized tonic-clonic seizure, not an absence seizure, and the context is a febrile event, making this mechanism irrelevant. *Increasing duration of Cl− channel opening* - This is the mechanism of action for **benzodiazepines** (e.g., lorazepam, diazepam), which are used to terminate **active seizures** by enhancing GABAergic inhibition [3]. - The patient's seizure has already stopped spontaneously, and he is awake and alert, so immediate administration of a benzodiazepine is not indicated for acute seizure termination.

Question 368: Shortest acting local anaesthetic

A. Dibucaine
B. Procaine
C. Chloroprocaine (Correct Answer)
D. Cocaine

Explanation: ***Chloroprocaine*** - **Chloroprocaine** is known for its rapid onset and very **short duration of action**, typically lasting 30-60 minutes, due to its **rapid hydrolysis** by plasma and liver esterases. - Its quick metabolism makes it suitable for short procedures where a brief blockade is desired, minimizing the risk of systemic toxicity. *Dibucaine* - **Dibucaine** is a local anesthetic with a **long duration of action**, typically 2 to 4 hours, which is much longer than chloroprocaine. - It is used topically and in spinal anesthesia, but its prolonged effect makes it unsuitable as the shortest-acting option. *Procaine* - **Procaine** is an ester-type local anesthetic with a relatively **short duration of action** (approximately 30-60 minutes), but it is generally longer than that of chloroprocaine. - It was one of the first synthetic local anesthetics and is less potent and shorter-acting than many modern agents. *Cocaine* - **Cocaine** has a moderate duration of action as a local anesthetic, typically lasting 60-90 minutes, which is longer than chloroprocaine. - While it is a potent local anesthetic and vasoconstrictor, its high abuse potential and systemic side effects limit its clinical use, mainly to topical application in otolaryngology.

Question 369: Drug used in osteoarthritis

A. Sulfasalazine
B. All of the options
C. Methotrexate
D. Glucosamine (Correct Answer)

Explanation: ***Correct: Glucosamine*** - **Glucosamine** is a common dietary supplement often used to treat **osteoarthritis (OA)** symptoms, believed to help rebuild cartilage. - While its efficacy is debated, many patients report symptom relief, and it is considered relatively safe for OA management. *Incorrect: Sulfasalazine* - **Sulfasalazine** is a disease-modifying antirheumatic drug (DMARD) primarily used to treat inflammatory conditions like **rheumatoid arthritis (RA)** and **inflammatory bowel disease (IBD)**. - It is not indicated for the treatment of **osteoarthritis**, which is a degenerative joint disease rather than an inflammatory one. *Incorrect: Methotrexate* - **Methotrexate** is a powerful immunosuppressant and DMARD used in conditions such as **rheumatoid arthritis (RA)**, **psoriasis**, and some cancers. - Its mechanism of action targets inflammation and immune responses, which are not the primary drivers of **osteoarthritis**, making it an inappropriate treatment. *Incorrect: All of the options* - This option is incorrect because neither **Sulfasalazine** nor **Methotrexate** are primary treatments for osteoarthritis. - Only glucosamine is commonly associated with osteoarthritis treatment among the choices provided.

Question 370: NSAID used commonly for topical ocular use is

A. Ibuprofen
B. Ketorolac (Correct Answer)
C. Acetaminophen
D. Aceclofenac

Explanation: ***Ketorolac*** - **Ketorolac tromethamine** is a potent NSAID commonly formulated as an ophthalmic solution for topical ocular use. - It is effective in reducing **post-operative inflammation** and pain following ocular surgery, such as cataract extraction. *Ibuprofen* - While ibuprofen is a widely used oral NSAID, it is **not commonly available** or prescribed as a topical ophthalmic preparation. - Its primary use is for systemic pain and inflammation relief. *Acetaminophen* - **Acetaminophen (paracetamol)** is an analgesic and antipyretic but is classified as a non-opioid analgesic and generally **not considered an NSAID** due to its minimal anti-inflammatory properties through COX inhibition. - It is not used for topical ocular administration to treat inflammation. *Aceclofenac* - Aceclofenac is an NSAID used systemically for inflammatory conditions, but it is **not commonly formulated** or used as a topical ocular agent. - **Diclofenac**, a related NSAID, is available as an ophthalmic solution, but not aceclofenac.

Practice by Chapter

NSAIDs: Classification and Mechanism

Practice Questions

COX-2 Selective Inhibitors

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Acetaminophen (Paracetamol)

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Opioid Analgesics and Antagonists

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Drugs Used in Gout and Hyperuricemia

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Drugs Used in Rheumatoid Arthritis

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Disease-Modifying Antirheumatic Drugs

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Glucocorticoids as Anti-inflammatory Agents

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Migraine Therapeutics

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Neuropathic Pain Management

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