Acetaminophen (Paracetamol) — MCQs
Antidote for acetaminophen poisoning is?
Management of typical febrile seizures includes all except:
A patient presents to the emergency department with a history of ingestion of ten tablets of paracetamol. He has developed oliguria and liver function tests show deranged values. In the context of paracetamol overdose, which of the following can be used in the management of this condition?
Both hepatic and renal failures can be caused by which of the following:
Mechanism of action of aspirin in pain relief is:
What is the treatment of choice for Lalita, a 26-year-old female who accidentally took 100 tablets of paracetamol?
Which of the following is a false statement?
A 55-year-old patient with gout has high uric acid levels; which drug should be avoided?
Which of the following is NOT an indication for the use of NSAIDs?
What is the mechanism of action of Aspirin?
Acetaminophen (Paracetamol) Indian Medical PG Practice Questions and MCQs
Question 1: Antidote for acetaminophen poisoning is?
- A. Penicillamine
- B. N-Acetyl cysteine (Correct Answer)
- C. Glycolamine
- D. Fomepizole
Explanation: ***N-Acetyl cysteine*** - **N-acetyl cysteine (NAC)** is the specific antidote for acetaminophen (paracetamol) poisoning, acting by replenishing hepatic **glutathione stores**. - **Glutathione** is crucial for detoxifying the toxic metabolite **N-acetyl-p-benzoquinone imine (NAPQI)**, preventing liver damage. *Penicillamine* - **Penicillamine** is a chelating agent used primarily in conditions like **Wilson's disease** (copper toxicity) and **rheumatoid arthritis**. - It has no role in the treatment or detoxification of **acetaminophen poisoning**. *Glycolamine* - **Glycolamine** is not a recognized pharmaceutical antidote for any specific poisoning. - This compound is not therapeutically relevant in toxicology scenarios, particularly for **acetaminophen overdose**. *Fomipezole* - **Fomepizole** is an antidote used for poisoning by **methanol** and **ethylene glycol**, not acetaminophen. - It works by inhibiting **alcohol dehydrogenase**, preventing the formation of toxic metabolites from these alcohols.
Question 2: Management of typical febrile seizures includes all except:
- A. Intermittent diazepam
- B. Sponging
- C. Paracetamol or ibuprofen
- D. Prophylactic phenobarbitone (Correct Answer)
Explanation: ***Prophylactic phenobarbitone*** - **Continuous prophylactic anticonvulsant therapy** with phenobarbitone is **definitively NOT recommended** for typical (simple) febrile seizures - The risks of chronic anticonvulsant use—including **sedation, cognitive impairment, and behavioral problems**—significantly outweigh any potential benefits - Evidence shows prophylactic phenobarbital does **not prevent future epilepsy** and has insufficient benefit in preventing recurrent febrile seizures - This is the **correct answer** as it is explicitly excluded from management guidelines *Intermittent diazepam* - While **not routinely recommended** for typical febrile seizures, intermittent rectal or buccal diazepam may be discussed as a *potential option* for specific situations (frequent recurrences, parental anxiety, prolonged seizures) - It serves as **rescue medication** to abort an ongoing seizure rather than daily prophylaxis - Its role in typical febrile seizure management is controversial and limited, but it may be mentioned in comprehensive management discussions *Sponging* - **Tepid sponging** is a supportive physical cooling measure used in fever management - While it does not prevent febrile seizures, it is part of general **symptomatic care** for fever reduction - Typically used alongside antipyretics to help lower body temperature and improve comfort *Paracetamol or ibuprofen* - **Antipyretics** are standard management for fever control and improving the child's comfort - While they do **not reliably prevent** febrile seizures from occurring, they are essential for **symptomatic fever management** - Recommended as first-line treatment for fever in children with febrile seizures
Question 3: A patient presents to the emergency department with a history of ingestion of ten tablets of paracetamol. He has developed oliguria and liver function tests show deranged values. In the context of paracetamol overdose, which of the following can be used in the management of this condition?
- A. N-acetylcysteine (Correct Answer)
- B. Dopamine
- C. Ursodeoxycholic acid
- D. Furosemide
Explanation: **Correct: N-acetylcysteine** - **N-acetylcysteine (NAC)** is the specific antidote for **paracetamol overdose**, working by replenishing **glutathione** stores in the liver. - Replenishing **glutathione** helps detoxify the toxic metabolite **N-acetyl-p-benzoquinone imine (NAPQI)**, preventing further **hepatic damage** and facilitating recovery in cases of **liver failure** and potential **renal damage** (oliguria). - Most effective when given within **8 hours** of ingestion, but remains beneficial even with **established hepatotoxicity** (as in this case with deranged LFTs). *Incorrect: Dopamine* - **Dopamine** is a **vasopressor** primarily used to increase **blood pressure** and **cardiac output** in conditions like **shock**. - While it might be used to support circulation in severe overdose complications, it does not directly treat the **paracetamol toxicity** itself. *Incorrect: Ursodeoxycholic acid* - **Ursodeoxycholic acid (UDCA)** is a **cholagogue** used in the management of **cholestatic liver diseases** (e.g., primary biliary cholangitis) by improving bile flow. - It has no role in the direct management of **acute liver failure** due to **paracetamol overdose**. *Incorrect: Furosemide* - **Furosemide** is a **loop diuretic** used to increase **urine output** in conditions like **fluid overload** or **heart failure**. - While **oliguria** is present, it is often a sign of **acute kidney injury** requiring supportive care, and furosemide would not address the underlying **toxic mechanism** of paracetamol.
Question 4: Both hepatic and renal failures can be caused by which of the following:
- A. Carbon tetrachloride
- B. Arsenic
- C. Paracetamol toxicity
- D. Copper sulphate (Correct Answer)
Explanation: ***Copper sulphate*** - **Copper sulphate poisoning** can lead to systemic toxicity, including severe **hepatic dysfunction** due to direct damage to hepatocytes and diffuse **renal tubular necrosis**, causing acute kidney injury. - Its corrosive nature also causes **gastrointestinal bleeding** and hemolysis, further contributing to multi-organ failure. *Carbon tetrachloride* - Primarily known for causing severe **hepatic necrosis** through its conversion to highly reactive free radicals, particularly in occupational exposures. - While it can induce some renal damage, **liver failure** is its most prominent and direct organ toxicity. *Arsenic* - **Arsenic poisoning** is associated with multi-organ effects, including dermatological, neurological, and cardiovascular issues. - It can cause **acute kidney injury** (typically through ATN) and some liver damage (hepatomegaly, jaundice), but its dominant toxicities are often broader and less specifically targeted to both organs in tandem compared to severe copper poisoning. *Paracetamol toxicity* - Overdose of paracetamol predominantly causes **acute liver failure** due to the depletion of glutathione and accumulation of toxic metabolites (NAPQI). - While severe liver failure can secondarily lead to **renal dysfunction** (hepatorenal syndrome), direct primary renal toxicity is less common than with copper sulphate.
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: What is the treatment of choice for Lalita, a 26-year-old female who accidentally took 100 tablets of paracetamol?
- A. Acetyl cysteine (Correct Answer)
- B. Gastric lavage
- C. Hemodialysis
- D. Alkaline diuresis
Explanation: ***Acetyl cysteine*** - **Acetyl cysteine** is the **antidote** of choice for paracetamol (acetaminophen) overdose. - It works by replenishing **glutathione stores**, which are essential for detoxifying the toxic metabolite of paracetamol, **N-acetyl-p-benzoquinone imine (NAPQI)**. *Gastric lavage* - **Gastric lavage** is generally not recommended for paracetamol overdose unless performed within **1 hour** of ingestion, and even then, its effectiveness is limited. - It carries risks such as aspiration and esophageal injury, making it less favorable than activated charcoal. *Hemodialysis* - **Hemodialysis** is generally reserved for severe cases of paracetamol overdose with life-threatening complications like **severe metabolic acidosis** or **renal failure**, and when acetyl cysteine treatment is delayed or ineffective. - Paracetamol itself is dialyzable, but hemodialysis is not the primary treatment for uncomplicated overdose. *Alkaline diuresis* - **Alkaline diuresis** is a treatment used for overdoses of **weak acids**, such as salicylates or phenobarbital, to enhance their renal excretion. - Paracetamol is not a weak acid, so alkaline diuresis would not be effective in eliminating it from the body.
Question 7: Which of the following is a false statement?
- A. Gastric irritation is more severe with NSAIDs compared to aspirin (Correct Answer)
- B. Acetaminophen does not have anti-inflammatory action
- C. Selective COX-2 inhibitors are contraindicated in postoperative patients
- D. Naproxen has the least cardiovascular risk among NSAIDs
Explanation: ***Gastric irritation is more severe with NSAIDs compared to aspirin*** - This statement is **false**. While both NSAIDs and aspirin can cause gastric irritation, **aspirin generally causes more severe gastric irritation** than most NSAIDs. - Aspirin causes significant GI toxicity due to its **direct irritant effect** on gastric mucosa and **irreversible inhibition of COX-1**, leading to reduced protective gastric mucus and bicarbonate secretion. - While NSAIDs also inhibit COX-1 causing gastric side effects, their direct irritant effect is typically less pronounced than aspirin. *Selective COX-2 inhibitors are contraindicated in postoperative patients* - This statement is **true**. **Selective COX-2 inhibitors** (coxibs like celecoxib, rofecoxib) are contraindicated or used with extreme caution in postoperative patients. - They increase risk of **cardiovascular thrombotic events** (MI, stroke) by disrupting the prostacyclin-thromboxane balance. - Postoperative patients have elevated cardiovascular risk, making selective COX-2 inhibitors particularly problematic in this setting. *Acetaminophen does not have anti-inflammatory action* - This statement is **true**. Acetaminophen (paracetamol) is primarily an **analgesic** and **antipyretic** agent. - It has **minimal to no anti-inflammatory effects** at therapeutic doses, unlike NSAIDs. - Its mechanism of action is predominantly **central** (CNS-based), with weak peripheral COX inhibition that does not translate to clinically significant anti-inflammatory activity. *Naproxen has the least cardiovascular risk among NSAIDs* - This statement is **true**. Among traditional NSAIDs, **naproxen is associated with the lowest cardiovascular risk**. - Studies suggest naproxen may have neutral or even slightly cardioprotective effects compared to other NSAIDs. - This is attributed to its relatively balanced and sustained COX-1/COX-2 inhibition, causing less disruption of the prostacyclin-thromboxane balance.
Question 8: A 55-year-old patient with gout has high uric acid levels; which drug should be avoided?
- A. Probenecid
- B. Allopurinol
- C. Febuxostat
- D. Aspirin (Correct Answer)
Explanation: ***Aspirin*** - High doses of **aspirin** can increase serum uric acid levels, which is detrimental for a patient with gout desiring to lower uric acid. - While low-dose aspirin (<300 mg/day) might have a minor uricosuric effect, higher doses are **anti-uricosuric** and should generally be avoided in gout. *Probenecid* - **Probenecid** is a **uricosuric agent** that helps excrete uric acid via the kidneys, making it beneficial for patients who underexcrete uric acid. - It works by inhibiting the reabsorption of uric acid in the renal tubules, thereby lowering serum uric acid levels. *Allopurinol* - **Allopurinol** is a **xanthine oxidase inhibitor** that reduces the production of uric acid by blocking the enzyme responsible for its synthesis. - It is a cornerstone treatment for chronic gout to lower uric acid levels and prevent recurrent attacks. *Febuxostat* - **Febuxostat** is also a **xanthine oxidase inhibitor**, similar to allopurinol, used to reduce uric acid production. - It is often considered an alternative for patients who cannot tolerate allopurinol or who do not achieve target uric acid levels with allopurinol.
Question 9: Which of the following is NOT an indication for the use of NSAIDs?
- A. As an analgesic
- B. In peptic ulcer disease (Correct Answer)
- C. Rheumatoid arthritis
- D. Osteoarthritis
Explanation: **Explanation:** The correct answer is **B. In peptic ulcer disease**. NSAIDs are generally **contraindicated** in patients with peptic ulcers because they inhibit the enzyme Cyclooxygenase-1 (COX-1). COX-1 is responsible for synthesizing cytoprotective prostaglandins ($PGE_2$ and $PGI_2$) in the gastric mucosa. These prostaglandins reduce gastric acid secretion, increase bicarbonate production, and maintain mucosal blood flow. By inhibiting them, NSAIDs compromise the gastric mucosal barrier, leading to erosions, ulceration, and potential perforation or hemorrhage. **Why the other options are incorrect:** * **A. As an analgesic:** NSAIDs are first-line agents for mild-to-moderate pain (e.g., headache, dysmenorrhea, or post-operative pain) by inhibiting $PGE_2$ synthesis, which sensitizes pain receptors. * **C & D. Rheumatoid Arthritis and Osteoarthritis:** NSAIDs are mainstay symptomatic treatments for these conditions. They reduce joint inflammation, swelling, and stiffness by inhibiting COX-2 at the site of inflammation. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Gastric Injury:** NSAIDs cause damage via two pathways: systemic inhibition of protective prostaglandins and direct local irritation (topical effect). * **Prophylaxis:** If an NSAID must be used in a high-risk patient, **Misoprostol** (a $PGE_1$ analog) or a Proton Pump Inhibitor (PPI) is co-administered for mucosal protection. * **Selective COX-2 Inhibitors (e.g., Celecoxib):** These carry a lower risk of GI ulcers but are associated with increased cardiovascular risks. * **Aspirin Sensitivity:** NSAIDs can trigger "Aspirin-Exacerbated Respiratory Disease" (AERD) in asthmatic patients due to a shift in arachidonic acid metabolism toward the leukotriene pathway.
Question 10: What is the mechanism of action of Aspirin?
- A. Inhibition of PGI2 formation
- B. Inhibition of TXA2 formation (Correct Answer)
- C. Stimulation of TXA2 formation
- D. Stimulation of platelet aggregation
Explanation: **Explanation:** **Mechanism of Action:** Aspirin (Acetylsalicylic acid) acts by **irreversibly inhibiting the enzyme Cyclooxygenase (COX-1 and COX-2)** via acetylation of a serine residue. In platelets, this leads to the inhibition of **Thromboxane A2 (TXA2)** synthesis. Since platelets are anucleated and cannot synthesize new enzymes, the inhibition lasts for the entire lifespan of the platelet (approx. 7–10 days). TXA2 is a potent vasoconstrictor and platelet aggregator; thus, its inhibition results in an anti-thrombotic effect. **Analysis of Options:** * **Option B (Correct):** Aspirin reduces TXA2 levels, which is the primary mechanism for its use in secondary prophylaxis of MI and stroke. * **Option A (Incorrect):** While aspirin can inhibit PGI2 (Prostacyclin) in vascular endothelium, PGI2 is a vasodilator and anti-aggregatory agent. At low doses, aspirin selectively inhibits TXA2 more than PGI2 because endothelial cells can regenerate COX enzymes, unlike platelets. * **Option C & D (Incorrect):** Aspirin inhibits, rather than stimulates, TXA2 formation. Consequently, it inhibits (rather than stimulates) platelet aggregation. **High-Yield NEET-PG Pearls:** 1. **Low-dose Aspirin (75–150 mg):** Exhibits anti-platelet effects (selective TXA2 inhibition). 2. **Zero-order Kinetics:** Aspirin follows zero-order elimination at high/toxic doses. 3. **Reye’s Syndrome:** Aspirin is contraindicated in children with viral infections (Varicella/Influenza) due to the risk of hepatic encephalopathy. 4. **Aspirin Triad (Samter’s Triad):** Asthma, Nasal polyposis, and Aspirin hypersensitivity. 5. **Antidote:** There is no specific antidote; treatment for toxicity involves gastric lavage and **urinary alkalinization** (using Sodium Bicarbonate) to enhance excretion.
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