Non-opioid Analgesics — MCQs
Which gene is responsible for the production of COX type 3?
A 50-year-old patient with renal insufficiency was recently operated on for pyelolithotomy. Which drug is the most appropriate choice for post-operative analgesia?
Which of the following diuretics is contraindicated in Hepatic coma?
Among NSAIDs, aspirin is unique because it:
Anti-inflammatory action of steroids is due to
The antidote of paracetamol poisoning
A female, Lalita, aged 26 years takes 100 tablets of paracetamol. Treatment of choice is:
Which of the following can be safely given in a kidney patient?
Which of the following is a false statement?
Which of the following agents is used for the treatment of post operative shivering?
Non-opioid Analgesics Indian Medical PG Practice Questions and MCQs
Question 1: Which gene is responsible for the production of COX type 3?
- A. COX 3 gene
- B. COX 2 gene
- C. None of the above
- D. COX I gene (Correct Answer)
Explanation: ***COX I gene*** - COX-3 is an **alternatively spliced variant** of the **COX-1 gene** (specifically, a splice variant of the COX-1 mRNA that retains intron 1). - While it was initially thought to be a distinct gene, research has shown that it arises from the same genetic locus as COX-1. *COX 2 gene* - The COX-2 gene encodes for the **inducible cyclooxygenase enzyme**, which is responsible for prostaglandin synthesis during inflammation. - It is a separate gene from COX-1 and has distinct regulatory mechanisms and physiological roles. *COX 3 gene* - There is currently **no distinct gene in humans** specifically identified as "COX-3". - COX-3 refers to a protein isoform derived from the COX-1 gene, not a separate genetic locus. *None of the above* - This option is incorrect because COX-3 is indeed derived from the **COX-1 gene** through alternative splicing. - The existence of COX-3 as a distinct protein product has been demonstrated, although its precise physiological role in humans is still under investigation.
Question 2: A 50-year-old patient with renal insufficiency was recently operated on for pyelolithotomy. Which drug is the most appropriate choice for post-operative analgesia?
- A. Diclofenac sodium
- B. Naproxen
- C. Indomethacin
- D. Acetaminophen (Correct Answer)
- E. Ketorolac
Explanation: ***Acetaminophen*** - **Acetaminophen** is primarily metabolized in the liver, with minimal renal excretion, making it a safer option for patients with **renal insufficiency**. - It provides effective **analgesia** without the adverse renal effects associated with NSAIDs. *Diclofenac sodium* - **Diclofenac** is a non-steroidal anti-inflammatory drug (**NSAID**) that can impair renal function, especially in patients with pre-existing **renal insufficiency**, by inhibiting prostaglandin synthesis. - Its use can lead to further **kidney damage** or exacerbate existing renal impairment. *Naproxen* - **Naproxen** is an **NSAID** that carries a significant risk of causing acute kidney injury in patients with **compromised renal function**. - It reduces renal blood flow and glomerular filtration rate, making it unsuitable for this patient. *Indomethacin* - **Indomethacin** is a potent **NSAID** known for its adverse renal effects, including acute renal failure. - It should be avoided in patients with **renal insufficiency** due to its potential to further decline kidney function. *Ketorolac* - **Ketorolac** is a potent **NSAID** commonly used for post-operative pain but is **contraindicated** in patients with renal insufficiency. - It has significant nephrotoxic potential and can cause acute renal failure, especially in patients with pre-existing kidney disease.
Question 3: Which of the following diuretics is contraindicated in Hepatic coma?
- A. Bumetanide
- B. Furosemide
- C. Acetazolamide (Correct Answer)
- D. Spironolactone
Explanation: ***Acetazolamide*** - **Acetazolamide** inhibits carbonic anhydrase, leading to increased bicarbonate excretion and metabolic acidosis. In patients with **hepatic coma**, this can worsen the condition by impairing the liver's ability to convert ammonia to urea, leading to increased levels of **ionized ammonia** that can cross the blood-brain barrier. - The resulting **metabolic acidosis** can also interfere with the kidney's response to ammonia, further exacerbating the **hepatic encephalopathy**. *Bumetanide* - **Bumetanide** is a loop diuretic that acts on the **thick ascending limb of the loop of Henle** to inhibit sodium, potassium, and chloride reabsorption. - It does not directly exacerbate **hepatic encephalopathy** through metabolic acidosis in the same way as acetazolamide. *Furosemide* - **Furosemide** is a loop diuretic similar to bumetanide, acting on the **thick ascending limb** to promote diuresis. - While aggressive diuresis with furosemide in critical patients can sometimes lead to **volume depletion** and electrolyte imbalances that may indirectly affect liver function, it does not directly worsen **hepatic coma** by altering systemic acid-base balance and ammonia detoxification like acetazolamide. *Spironolactone* - **Spironolactone** is an **aldosterone antagonist** and a potassium-sparing diuretic, commonly used in liver cirrhosis with ascites. - It does not directly cause **metabolic acidosis** or increase ionized ammonia levels; in fact, by improving fluid balance, it can sometimes help manage complications of liver disease.
Question 4: Among NSAIDs, aspirin is unique because it:
- A. Irreversibly inhibits its target enzyme (Correct Answer)
- B. Reduces fever
- C. Selectively inhibits COX-1 enzyme
- D. May reduce the risk of colon cancer
Explanation: ***Irreversibly inhibits its target enzyme*** - Aspirin uniquely acetylates a **serine residue** on both **COX-1 and COX-2**, permanently inactivating the enzyme. - This irreversible inhibition is why aspirin's antiplatelet effects last for the lifespan of the platelet (7-10 days), unlike other NSAIDs which are reversible inhibitors. *May reduce the risk of colon cancer* - While some studies suggest a link between long-term aspirin use and reduced colon cancer risk, this is a property shared by some other NSAIDs and is not a unique distinguishing feature of aspirin among NSAIDs. - This effect is generally attributed to the **inhibition of COX-2**, which is involved in tumor growth and inflammation. *Reduces fever* - **Antipyresis** (fever reduction) is a characteristic effect of nearly all NSAIDs, including ibuprofen and naproxen, due to the inhibition of prostaglandin synthesis in the hypothalamus. - Therefore, this is not a unique feature of aspirin. *Selectively inhibits COX-1 enzyme* - Aspirin is a **non-selective COX inhibitor**, meaning it inhibits both COX-1 and COX-2 enzymes at anti-inflammatory doses. - While it has a higher affinity for COX-1 at low doses, drugs like celecoxib are genuinely selective COX-2 inhibitors, and no common NSAID is purely selective for COX-1.
Question 5: 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 6: The antidote of paracetamol poisoning
- A. Sodium bicarbonate
- B. Flumazenil
- C. N-acetyl cysteine (Correct Answer)
- D. Naloxone
Explanation: ***N-acetyl cysteine*** - **N-acetyl cysteine (NAC)** is the specific antidote for **paracetamol (acetaminophen)** overdose. - NAC works by replenishing **glutathione stores** in the liver, which are crucial for detoxifying the toxic metabolite **N-acetyl-p-benzoquinone imine (NAPQI)**. *Sodium bicarbonate* - **Sodium bicarbonate** is used to treat **metabolic acidosis** and certain drug overdoses that cause cardiac toxicity, such as tricyclic antidepressants. - It does not have a direct role in detoxifying paracetamol or its metabolites. *Flumazenil* - **Flumazenil** is an antagonist at the **benzodiazepine receptor** and is used to reverse the sedative effects of benzodiazepine overdose. - It has no effect on paracetamol toxicity. *Naloxone* - **Naloxone** is an **opioid receptor antagonist** used to reverse the effects of opioid overdose. - It does not interact with the metabolic pathways or toxic effects of paracetamol.
Question 7: A female, Lalita, aged 26 years takes 100 tablets of paracetamol. Treatment of choice is:
- A. Lavage with charcoal
- B. Dialysis
- C. Alkaline diuresis
- D. Acetylcysteine (Correct Answer)
Explanation: ***Acetylcysteine*** - **Acetylcysteine** is the **antidote of choice** for paracetamol (acetaminophen) overdose, replenishing **glutathione stores** and detoxifying toxic paracetamol metabolites. - Early administration (within 8 hours of ingestion) is crucial for preventing **hepatic damage**, as it inhibits the binding of the toxic metabolite **NAPQI** to liver proteins. *Lavage with charcoal* - **Gastric lavage** and **activated charcoal** are primarily used for **decontamination** in the early stages (within 1-2 hours) of acute overdose, to prevent absorption. - Given the ingestion of **100 tablets**, a significant amount of paracetamol has likely already been absorbed, making these less effective as the sole treatment. *Dialysis* - **Dialysis** is generally reserved for severe cases of paracetamol overdose complicated by **acute liver failure** or other severe organ dysfunction, which requires elimination of paracetamol and its metabolites from the blood. - It is not the **first-line treatment** for acute paracetamol overdose itself, but rather a supportive measure for complications. *Alkaline diuresis* - **Alkaline diuresis** is sometimes used to enhance the elimination of **acidic drugs** like salicylates (aspirin) from the body. - Paracetamol is primarily metabolized by the liver into glucuronide and sulfate conjugates, which are then excreted, and its elimination is not significantly enhanced by **alkaline diuresis**.
Question 8: Which of the following can be safely given in a kidney patient?
- A. Ibuprofen
- B. Ketorolac
- C. Acetyl salicylic acid
- D. Fluconazole (Correct Answer)
Explanation: ***Fluconazole*** - Fluconazole **can be safely given in kidney patients with appropriate dose adjustment** based on the patient's **creatinine clearance**. - It is primarily cleared renally (80% unchanged in urine), so dose reduction is necessary to prevent accumulation and toxicity in patients with impaired kidney function. - Unlike NSAIDs, fluconazole does not directly harm the kidneys or reduce renal blood flow, making it a safer choice when dose-adjusted appropriately. *Ibuprofen* - **NSAIDs** like **ibuprofen** are generally avoided in kidney patients due to their potential to cause **acute kidney injury (AKI)** by inhibiting prostaglandin synthesis, leading to renal vasoconstriction. - They can worsen existing kidney disease or induce new onset kidney damage, especially in patients with compromised renal function. - Risk of **hyperkalemia**, **fluid retention**, and **worsening of hypertension** in CKD patients. *Ketorolac* - **Ketorolac** is a potent **NSAID** that is **contraindicated in patients with renal impairment** (CrCl <50 mL/min). - Its use can lead to significant **renal vasoconstriction** and reduction in **glomerular filtration rate (GFR)**, posing a high risk for **acute kidney injury**. - Has the highest risk of renal adverse effects among commonly used NSAIDs. *Acetylsalicylic acid* - **Acetylsalicylic acid (aspirin)** at analgesic/anti-inflammatory doses can be harmful to kidney patients. - Like other NSAIDs, it can inhibit **renal prostaglandins**, leading to decreased renal blood flow and potential for **kidney damage**. - While low-dose aspirin (75-100mg) for cardioprotection may be used cautiously in stable CKD, higher doses should be avoided.
Question 9: 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 10: Which of the following agents is used for the treatment of post operative shivering?
- A. Atropine
- B. Thiopentone
- C. Pethidine (Correct Answer)
- D. Suxamethonium
Explanation: ***Pethidine*** - **Pethidine (meperidine)** is a **synthetic opioid** known for its **mu-receptor agonism** and weak anticholinergic properties, making it effective in treating **post-operative shivering**. - Its mechanism in reducing shivering is thought to involve modulation of the **thermoregulatory center** in the hypothalamus. *Atropine* - **Atropine** is an **anticholinergic drug** that primarily blocks muscarinic acetylcholine receptors, leading to effects like increased heart rate and decreased secretions. - It does not directly act on the thermoregulatory centers or muscle activity responsible for shivering. *Thiopentone* - **Thiopentone** is a **barbiturate** used as an intravenous anesthetic, primarily for induction of anesthesia. - While it has CNS depressant effects, it is not indicated or effective for the specific treatment of post-operative shivering. *Suxamethonium* - **Suxamethonium (succinylcholine)** is a **depolarizing neuromuscular blocker** used to induce muscle paralysis, typically for intubation. - It would prevent shivering by paralyzing skeletal muscles, but this is a dangerous and inappropriate treatment for shivering due to its profound respiratory depressant effects.
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