Clinical Pharmacology and Drug Toxicity — MCQs

Clinical Pharmacology and Drug Toxicity Indian Medical PG Practice Questions and MCQs

Question 771: Dicobalt EDTA is used as an antidote for which poisoning?

A. Mushroom
B. Lead
C. Cyanide (Correct Answer)
D. Mercury

Explanation: Cyanide - **Dicobalt EDTA** acts as a **chelating agent** that specifically binds to cyanide ions, forming a stable, non-toxic complex that can be excreted from the body. - This binding prevents cyanide from inhibiting **cytochrome c oxidase** in the mitochondria, thus restoring cellular respiration. *Mushroom* - Treatment for mushroom poisoning is highly dependent on the **species of mushroom** and the toxins involved, and typically involves **supportive care**, activated charcoal, and specific antidotes like **silymarin** or **N-acetylcysteine** for certain types of Amanita poisoning. - Dicobalt EDTA is not indicated for any known form of mushroom toxicity. *Lead* - **Lead poisoning** is treated with **chelating agents** such as **EDTA (calcium disodium EDTA)**, **dimercaprol (BAL)**, or **succimer (DMSA)**, which bind to lead and promote its excretion [1], [2]. - Dicobalt EDTA is specifically formulated for cyanide and would not be effective or safe for lead poisoning due to its cobalt content. *Mercury* - **Mercury poisoning** is typically treated with **chelating agents** like **dimercaprol (BAL)**, **succimer (DMSA)**, or **D-penicillamine**, which help remove mercury from the body [3]. - Dicobalt EDTA does not have affinity for mercury and can be harmful if used for mercury poisoning.

Question 772: Which drug does NOT cause optic neuropathy?

A. Chloramphenicol
B. Penicillin (Correct Answer)
C. Ethambutol
D. INH

Explanation: ***Penicillin*** - Penicillin is a widely used antibiotic that is **not associated with optic neuropathy** - Its primary side effects are **allergic reactions and hypersensitivity** - Visual disturbances or optic nerve damage are **not characteristic** of penicillin therapy *Chloramphenicol* - Known to cause **dose-dependent and duration-dependent optic neuropathy**, especially with prolonged use - Can lead to visual impairment, including reduced visual acuity and color vision defects - May be **irreversible** in some cases *Ethambutol* - **Most notorious** antitubercular drug for causing optic neuritis - Causes **dose-dependent bilateral visual loss** and **red-green color blindness** - Requires regular visual monitoring during therapy - Potentially **irreversible** optic nerve damage *INH (Isoniazid)* - Can cause optic neuropathy, though **less frequently** than ethambutol - Usually associated with **high doses** or prolonged therapy - Risk increases in slow acetylators and those with nutritional deficiencies

Question 773: Diazepam poisoning is treated by:

A. Resins
B. Hemofiltration
C. Charcoal
D. Flumazenil (Correct Answer)

Explanation: ***Flumazenil*** - **Flumazenil** is a **benzodiazepine receptor antagonist** that competitively binds to the benzodiazepine binding site on the GABA-A receptor, reversing the effects of diazepam. - It is used in cases of severe benzodiazepine overdose causing **respiratory depression** or **severe sedation**. *Resins* - **Resins**, such as **cholestyramine**, are typically used to bind toxins or drugs in the **gastrointestinal tract** that undergo enterohepatic recirculation. - They are generally not effective for reversing the central nervous system depression caused by a benzodiazepine overdose. *Hemofiltration* - **Hemofiltration** is a form of renal replacement therapy used to remove small and middle molecular weight substances from the blood. - While it can remove some drugs, **diazepam** is highly **lipophilic** and extensively **protein-bound**, making it poorly amenable to removal by hemofiltration. *Charcoal* - **Activated charcoal** is used to prevent the absorption of ingested toxins from the gastrointestinal tract. - It is effective when administered soon after ingestion but does not reverse the established effects of an absorbed drug like diazepam in an overdose situation.

Question 774: A patient was on lithium therapy for bipolar disorder for 6 months. She fasted for few days due to religious reasons and presented with coarse tremors, abdominal pain, nausea, dizziness & confusion. Which of the following should be done to assess her condition?

A. ECG
B. S. lithium levels (Correct Answer)
C. MRI
D. S. electrolytes

Explanation: ***S. lithium levels*** - The patient's symptoms (coarse tremors, abdominal pain, nausea, dizziness, confusion) are classic for **lithium toxicity**, which is exacerbated by **dehydration** from fasting [1], [2]. - Measuring **serum lithium levels** is crucial for confirming the diagnosis and guiding immediate management [1]. *ECG* - While lithium toxicity can cause **cardiac arrhythmias** (QT prolongation, T-wave changes), an ECG is a secondary assessment to evaluate for complications, not the primary diagnostic test for toxicity itself. - An ECG doesn't directly measure lithium concentration, which is essential for diagnosing toxicity. *S. electrolyte* - **Electrolyte imbalances**, particularly **hyponatremia**, can worsen lithium toxicity by affecting its renal excretion [2]. - While important to check for contributing factors and guide supportive care, measuring electrolytes is secondary to confirming elevated lithium levels as the cause of symptoms. *MRI* - An **MRI of the brain** is not indicated for the initial assessment of suspected lithium toxicity. - It would only be considered if there were concerns for focal neurological deficits or other structural brain abnormalities, which are not directly suggested by the presented symptoms of lithium toxicity.

Question 775: Anti-glaucoma drug that acts by increasing uveoscleral outflow is

A. Dorzolamide
B. Latanoprost (Correct Answer)
C. Pilocarpine
D. Timolol

Explanation: ***Latanoprost*** - **Latanoprost** is a **prostaglandin F2α analog** that effectively lowers intraocular pressure by significantly increasing **uveoscleral outflow**. - It works by remodeling the extracellular matrix in the ciliary body and sclera, which facilitates the drainage of aqueous humor through the uveoscleral pathway. *Dorzolamide* - **Dorzolamide** is a **topical carbonic anhydrase inhibitor** that reduces the production of aqueous humor, thus lowering intraocular pressure. - It does not directly affect the uveoscleral outflow pathway. *Pilocarpine* - **Pilocarpine** is a **cholinergic agonist** that primarily works by increasing the **trabecular outflow** of aqueous humor through contraction of the ciliary muscle [1]. - It does not significantly influence the uveoscleral outflow pathway. *Timolol* - **Timolol** is a **beta-adrenergic blocker** that reduces aqueous humor production by the ciliary body [1]. - Its mechanism of action involves decreasing the formation, rather than increasing the outflow, of aqueous humor [1].

Question 776: Antidote used in methyl alcohol poisoning is?

A. Alpha methyl dopa
B. Fomepizole (Correct Answer)
C. Acetyl cysteine
D. EDTA

Explanation: ***Fomepizole*** - **Fomepizole** acts as a competitive inhibitor of **alcohol dehydrogenase**, preventing the metabolism of **methanol** into toxic metabolites like **formic acid**. - This prevents the accumulation of highly toxic substances responsible for the metabolic acidosis, visual disturbances, and organ damage seen in **methanol poisoning**. *Alpha methyl dopa* - **Alpha-methyl dopa** is an antihypertensive drug that primarily acts as a central alpha-2 adrenergic agonist, reducing sympathetic outflow. - It is not used in the management of **methanol poisoning** and has no role in inhibiting alcohol metabolism. *Acetyl cysteine* - **Acetylcysteine** is primarily used as an antidote for **acetaminophen (paracetamol) overdose**, where it replenishes glutathione stores, and as a mucolytic agent. - It does not inhibit the metabolism of **methanol** nor does it have any direct therapeutic effect in **methanol poisoning**. *EDTA* - **EDTA (Ethylenediaminetetraacetic acid)** is a chelating agent used to treat **heavy metal poisoning**, such as lead poisoning. - It binds to metal ions, facilitating their excretion from the body, but has no role in the management of **methanol poisoning**.

Question 777: Treatment of dhatura poisoning is done with:

A. Physostigmine (Correct Answer)
B. Neostigmine
C. Naloxone
D. Pilocarpine

Explanation: ***Physostigmine*** - **Physostigmine** is a **reversible cholinesterase inhibitor** that can cross the **blood-brain barrier**, allowing it to counteract both peripheral and central anticholinergic effects of dhatura poisoning. - It increases the amount of **acetylcholine** at muscarinic and nicotinic receptors, directly competing with the anticholinergic agents. *Neostigmine* - **Neostigmine** is also a **cholinesterase inhibitor**, but it does not cross the **blood-brain barrier** effectively. - Therefore, it is primarily used for its **peripheral effects** and is not suitable for reversing the central nervous system manifestations of dhatura poisoning. *Naloxone* - **Naloxone** is a **pure opioid antagonist** used to reverse the effects of **opioid overdose**. - It has no role in the treatment of **dhatura poisoning**, which involves anticholinergic toxicity. *Pilocarpine* - **Pilocarpine** is a **direct muscarinic agonist** that acts at peripheral muscarinic receptors. - While it could counteract some peripheral anticholinergic effects, it does not cross the **blood-brain barrier** effectively and cannot address the central nervous system manifestations. - It is not the preferred or primary antidote for **anticholinergic toxicity** as it doesn't address both central and peripheral effects like physostigmine does.

Question 778: A 45 year old male, known case of Rheumatoid arthritis is on a monotherapy since many years. Symptoms of RA are controlled but suddenly patient develops blurring of vision. Which of the following drug is responsible for sudden effect on vision?

A. Methotrexate
B. Hydroxychloroquine (Correct Answer)
C. Sulfasalazine
D. Leflunomide

Explanation: ***Hydroxychloroquine*** - **Hydroxychloroquine** [1] is known to cause **retinal toxicity** (maculopathy) as a dose-dependent, long-term side effect, leading to **blurring of vision** and other visual disturbances. - Patients on long-term hydroxychloroquine therapy require regular **ophthalmological screening** to detect and prevent irreversible vision loss. *Methotrexate* - **Methotrexate** is a common DMARD used in RA [1], but its ocular side effects are typically rare and less severe, usually involving **conjunctivitis** or **periorbital edema**. - It does not commonly cause **maculopathy** or sudden profound blurring of vision. *Sulfasalazine* - **Sulfasalazine** [1] can cause a range of side effects, including gastrointestinal issues and various hypersensitivity reactions. - Ocular side effects are infrequent and generally mild, such as **conjunctivitis** or **periorbital edema**, and not severe blurring of vision due to retinal damage. *Leflunomide* - **Leflunomide** is an immunosuppressive DMARD [1] whose common adverse effects include hepatotoxicity, gastrointestinal upset, and hypertension. - Significant **ocular toxicity** leading to blurring of vision, particularly retinal damage, is not a characteristic side effect of **leflunomide**.

Question 779: Oximes are contraindicated in which poisoning:

A. Diazinon
B. Carbamate (Correct Answer)
C. Phorate
D. Malathion

Explanation: ***Carbamate*** - Traditionally, oximes were considered **contraindicated** in carbamate poisoning based on concerns they could worsen the **cholinergic crisis** by reactivating carbamylated acetylcholinesterase. - Carbamates spontaneously **decarbamylate** from acetylcholinesterase within minutes to hours, so their inhibition is typically **short-lived and reversible**. - **Clinical relevance**: While modern evidence suggests oximes are more likely **ineffective** rather than harmful in carbamate poisoning, they are generally **not recommended** as they provide no therapeutic benefit. For exam purposes, particularly in historical contexts (NEET 2012-2013), carbamate poisoning is the answer for oxime contraindication. *Diazinon* - Diazinon is an **organophosphate**, and oximes like pralidoxime are **strongly indicated** for reactivating **acetylcholinesterase** inhibited by organophosphates. - Oximes are a crucial part of recommended antidotal therapy alongside **atropine** for severe organophosphate poisoning. - Must be administered early (within 24-48 hours) before **aging** of the phosphorylated enzyme occurs. *Phorate* - Phorate is a highly toxic **organophosphate pesticide**, and oximes are **indicated** for treatment of phorate poisoning. - Oximes work by **dephosphorylating** (nucleophilic attack on) the acetylcholinesterase enzyme, which has been inhibited by the organophosphate, restoring its catalytic function. *Malathion* - Malathion is an **organophosphate insecticide**, and oxime reactivators are **effective** in malathion poisoning. - The mechanism involves **cleaving the phosphate bond** from the serine residue on the acetylcholinesterase enzyme, allowing it to metabolize acetylcholine again and reverse cholinergic toxicity.

Question 780: Acrodynia, or Pink disease, occurs in poisoning with which of the following substances?

A. Lead
B. Thallium
C. Arsenic
D. Mercury (Correct Answer)

Explanation: ***Mercury*** - **Acrodynia**, also known as **Pink disease**, is a rare and severe form of **mercury poisoning**, primarily affecting infants and young children. - Key symptoms include **pinkish-red rash** on the hands and feet, hypertension, irritability, profuse sweating, and muscle weakness. *Lead* - **Lead poisoning** typically presents with symptoms such as **abdominal pain**, constipation, developmental delay, and a **lead line on the gums**. - It does not cause the characteristic rash or other symptoms associated with acrodynia. *Thallium* - **Thallium poisoning** is known for causing **hair loss (alopecia)**, excruciating neuropathic pain, gastrointestinal disturbances, and neurological symptoms. - While it is a neurotoxic heavy metal, its clinical picture is distinct from acrodynia. *Arsenic* - **Arsenic poisoning** can manifest with dermatological signs like **hyperpigmentation** and **hyperkeratosis**, as well as gastrointestinal and neurological symptoms. - It does not produce the pinkish rash, irritability, or hypertension typical of acrodynia.

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Principles of Clinical Pharmacology

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Therapeutic Drug Monitoring

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Drug Toxicity and Overdose

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Antidotes and Their Applications

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Management of Drug Poisoning

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Drug-Induced Liver Injury

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Drug-Induced Kidney Injury

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Drug-Induced Blood Dyscrasias

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Drug-Induced QT Prolongation

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Pharmacovigilance

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