Clinical Pharmacology and Drug Toxicity Practice Questions

Q: Which of the following is NOT used for iron poisoning?

Penicillamine. ***Penicillamine*** - **Penicillamine** is a chelating agent indicated for **copper poisoning** (Wilson's disease), **lead poisoning**, and **rheumatoid arthritis**, but has **no role in iron poisoning**. - It works by chelating copper, lead, and other heavy metals, but does not effectively chelate iron. - This is the most clearly incorrect option as it is never indicated for iron toxicity. *EDTA (Ethylenediaminetetraacetic acid)* - **EDTA** is primarily used for **lead poisoning** and hypercalcemia. - While not routinely used for iron poisoning, it can form iron-EDTA complexes, which may paradoxically worsen toxicity. - **CaNa₂EDTA** is avoided in iron poisoning due to potential complications. *Desferrioxamine* - **Desferrioxamine (Deferoxamine)** is the **first-line antidote** for severe iron poisoning. - It is a highly specific iron-chelating agent that binds free iron in the bloodstream and promotes its renal excretion as ferrioxamine. - It reduces iron-mediated oxidative damage to organs (especially liver, heart, and GI tract). *Gastric lavage* - **Gastric lavage** can be used as a decontamination method in acute iron poisoning if performed early (within 1-2 hours of ingestion). - It helps remove unabsorbed iron tablets from the stomach, reducing further systemic absorption. - Whole bowel irrigation with polyethylene glycol is often preferred for iron tablet ingestion.

Q: All are features of organophosphorus poisoning, except:

Mydriasis. ***Mydriasis*** - Organophosphorus poisoning leads to excessive **acetylcholine** activity, causing **miosis** (pinpoint pupils), not mydriasis. - Mydriasis would indicate **anticholinergic** effects, which are opposite to the symptoms of organophosphorus poisoning. *Lacrimation* - Excess **acetylcholine** stimulates **muscarinic receptors** in lacrimal glands, leading to excessive tear production. - This is a classic "SLUDGE" symptom (Salivation, Lacrimation, Urination, Defecation, Gastric upset, Emesis). *Bradycardia* - Increased **acetylcholine** activity at cardiac muscarinic receptors (M2 receptors) slows the heart rate, causing **bradycardia**. - This is a common and potentially dangerous cardiovascular effect of organophosphorus poisoning. *Sweating* - **Acetylcholine** acts on muscarinic receptors in secretory glands, including sweat glands, causing profuse **sweating**. - This is another characteristic cholinergic symptom due to widespread autonomic overstimulation.

Q: All of the following can result in gynecomastia except:

Aromatase inhibitors. ***Aromatase inhibitors*** - **Aromatase inhibitors** block the conversion of androgens to estrogens, thereby **decreasing estrogen levels** which would prevent rather than cause gynecomastia. - They are used in estrogen-sensitive breast cancers to reduce estrogen-dependent growth. *Spironolactone* - **Spironolactone** is an aldosterone antagonist that also possesses anti-androgenic effects and can inhibit androgen synthesis, leading to an **increased estrogen-to-androgen ratio** and gynecomastia. - It can also directly stimulate the estrogen receptor in male breast tissue. *Sulphonamides* - Certain **sulphonamides**, particularly sulfasalazine, have been associated with gynecomastia, possibly due to direct toxic effects on testicular function leading to a **relative increase in estrogen activity**. - While less common than with some other drugs, it can alter the estrogen-androgen balance. *Digoxin* - **Digoxin** can cause gynecomastia by mimicking estrogen physiologically or by inhibiting androgen production, leading to an **alteration in the estrogen-to-androgen ratio**. - The risk of gynecomastia is especially noted with prolonged use and higher doses of digoxin.

Q: Which of the following is NOT considered a 'date rape drug'?

Propofol. ***Propofol*** - **Propofol** is an **intravenous anesthetic** and sedative primarily used in medical settings for induction and maintenance of anesthesia or for sedation in critical care. - While it can cause sedation and amnesia, it is not commonly associated with or used as a **'date rape drug'** due to its rapid onset and short duration of action, requiring medical administration. *Rohypnol* - **Rohypnol** (flunitrazepam) is a potent **benzodiazepine** known for its sedative-hypnotic effects and is commonly explicitly referred to as a **'date rape drug'**. - It can cause **amnesia**, muscle relaxation, and impaired judgment, making victims vulnerable and unable to recall events. *Ketamine* - **Ketamine** is a **dissociative anesthetic** that causes a trance-like state, pain relief, sedation, and amnesia, and is also known as a **'date rape drug'**. - At lower doses, it can produce **hallucinations** and a sense of detachment, impairing a person's ability to resist or remember. *Gamma hydroxyl butyrate* - **Gamma-hydroxybutyrate (GHB)** is a **central nervous system depressant** that has been widely implicated as a **'date rape drug'**. - It rapidly induces **sedation**, euphoria, and amnesia, with effects often lasting for several hours.

Q: Following are used in treatment of digitalis toxicity except-

Hemodialysis. ***Hemodialysis***\n - **Digoxin** has a **large volume of distribution (5-7 L/kg)** and is extensively bound to tissue proteins throughout the body.\n - Only a small fraction of digoxin remains in the plasma, making hemodialysis **ineffective** for removing significant amounts of the drug.\n - Hemodialysis is **not recommended** and **not used** as a treatment for digitalis toxicity.\n\n*Fab fragments*\n - **Digoxin-specific antibody fragments** (Digibind/DigiFab) directly bind to and neutralize free digoxin molecules.\n - This is the **gold standard treatment** for severe digitalis toxicity, especially with life-threatening arrhythmias or significant hyperkalemia.\n - Works rapidly to reverse toxic effects by binding digoxin in the serum.\n\n*Lignocaine*\n - **Lignocaine** (lidocaine) is a class IB antiarrhythmic used to treat **ventricular arrhythmias** caused by digitalis toxicity [1].\n - Suppresses ectopic ventricular activity without further depressing AV conduction.\n - Preferred over other antiarrhythmics like phenytoin for digoxin-induced ventricular tachyarrhythmias.\n\n*Potassium*\n - **Context-dependent use**: Potassium is used in digitalis toxicity **only when hypokalemia is present**.\n - **Hypokalemia** increases myocardial sensitivity to digoxin and worsens toxicity, so correction with potassium is therapeutic.\n - **Important contraindication**: Potassium is **contraindicated in acute digoxin overdose with hyperkalemia**, which commonly occurs due to Na-K-ATPase pump inhibition.\n - When appropriately indicated (hypokalemic state), potassium IS used in management of digitalis toxicity.

Q: Which of the properties accounts for ethanol's use in ethylene glycol poisoning?

Competitive inhibitor of alcohol dehydrogenase. ***Competitive inhibitor of alcohol dehydrogenase*** - **Ethanol** acts as a **competitive inhibitor** of **alcohol dehydrogenase (ADH)**, the enzyme responsible for metabolizing ethylene glycol into toxic metabolites. - By competing for ADH, ethanol prevents the formation of toxic compounds like **glycolic acid** and **oxalic acid**, which cause the severe acidosis and organ damage seen in ethylene glycol poisoning. *Competitive inhibitor of NADPH oxidase* - **NADPH oxidase** is an enzyme complex primarily involved in the production of **reactive oxygen species** during the respiratory burst in phagocytes, related to immune function. - This enzyme is not directly involved in the metabolism of ethylene glycol, so inhibiting it would not be a treatment for ethylene glycol poisoning. *Competitive inhibitor of aldehyde dehydrogenase* - **Aldehyde dehydrogenase (ALDH)** is an enzyme that metabolizes **acetaldehyde** (a product of ethanol metabolism) and other aldehydes, converting them into carboxylic acids. - While ALDH is involved in alcohol metabolism, it is not the primary enzyme responsible for the initial metabolism of ethylene glycol into its toxic byproducts, which is the target for treatment. *Non-competitive inhibitor of aldehyde dehydrogenase* - Non-competitive inhibition of **aldehyde dehydrogenase (ALDH)** would primarily affect the metabolism of other aldehydes, including those produced from ethanol breakdown, leading to an accumulation of aldehydes (e.g., acetaldehyde). - This mechanism would not prevent the initial formation of toxic metabolites from ethylene glycol, which is the goal of therapy in ethylene glycol poisoning.

Q: Which one of the following drugs cannot cause Pseudotumor Cerebri ?

Metformin. ***Metformin*** - **Metformin** is an oral hypoglycemic agent used for **type 2 diabetes** and is not associated with pseudotumor cerebri. - There is no known mechanism by which metformin would increase **intracranial pressure**. *Nitrofurantoin* - **Nitrofurantoin**, an antibiotic used for urinary tract infections, has been rarely implicated in drug-induced **pseudotumor cerebri**. - It works by interfering with **bacterial enzyme systems**, not typically affecting host intracranial fluid dynamics directly, but can cause idiosyncratic reactions. *Tetracycline* - **Tetracycline-class antibiotics** are well-known causes of **pseudotumor cerebri** (idiopathic intracranial hypertension). - This effect is thought to be dose-dependent and related to interference with **cerebrospinal fluid (CSF) absorption** or production. *Nalidixic acid* - **Nalidixic acid**, a quinolone antibiotic, is also recognized as a cause of **pseudotumor cerebri**, particularly in children. - Its mechanism is not fully understood but is believed to involve disturbances in **CSF dynamics**.

Q: All of the following are adverse effects of thalidomide except:

Myocarditis. ***Myocarditis*** - **Myocarditis** is not an established adverse effect of thalidomide in standard pharmacology references. - While thalidomide can cause cardiovascular effects such as **bradycardia** and **thromboembolic events**, direct myocardial inflammation is not a recognized complication. - This is the correct answer as it is NOT an adverse effect of thalidomide. *Constipation* - **Constipation** is a very common gastrointestinal side effect of thalidomide due to its **anticholinergic-like effects**. - Patients often require proactive management with laxatives to mitigate this side effect. *Peripheral neuropathy* - **Peripheral neuropathy** is the most significant and dose-limiting adverse effect of thalidomide, often presenting as **sensory deficits** in a stocking-glove distribution. - It can be **irreversible** and may necessitate discontinuation of the drug. - This is a major concern requiring regular monitoring during treatment. *Sedation* - **Sedation** and **drowsiness** are common adverse effects of thalidomide due to its **central nervous system depressant properties**. - This effect often leads to administration before bedtime to minimize impact on daily activities.

Q: Adverse reactions following whole-cell pertussis immunization include:

All of the options. ***All of the options*** are well-documented adverse reactions following whole-cell pertussis immunization. *Fever* - **Fever** is a common systemic adverse reaction following whole-cell pertussis immunization, occurring in **10-50%** of recipients - It usually presents within the first **24-48 hours** after vaccination due to the immunostimulatory components of the vaccine - Generally mild and self-limiting, resolving within 1-2 days *Anaphylaxis* - **Anaphylaxis** is a rare but severe allergic reaction that can occur after whole-cell pertussis vaccination (approximately **1 in 1,000,000** doses) - It is an **IgE-mediated type I hypersensitivity reaction** requiring immediate medical intervention with intramuscular epinephrine - Usually occurs within **minutes to hours** after vaccination *Local swelling* - **Local swelling** at the injection site is a very common adverse reaction, occurring in **>50%** of recipients - This reaction is typically mild, localized to the injection site, and represents a normal inflammatory response - Usually resolves spontaneously within **2-3 days** without specific treatment

Question 1

Which of the following is NOT used for iron poisoning?

Accepted Answer

Penicillamine

Answer

EDTA (Ethylenediaminetetraacetic acid)

Answer

Desferrioxamine

Answer

Gastric lavage

Question 2

All are features of organophosphorus poisoning, except:

Accepted Answer

Mydriasis

Answer

Lacrimation

Answer

Bradycardia

Answer

Sweating

Question 3

All of the following can result in gynecomastia except:

Accepted Answer

Aromatase inhibitors

Answer

Spironolactone

Answer

Digoxin

Answer

Sulphonamides

Question 4

Which of the following is NOT considered a 'date rape drug'?

Accepted Answer

Propofol

Answer

Rohypnol

Answer

Ketamine

Answer

Gamma hydroxyl butyrate

Question 5

Following are used in treatment of digitalis toxicity except-

Accepted Answer

Hemodialysis

Answer

Fab fragments

Answer

Lignocaine

Answer

Potassium

Question 6

Which of the properties accounts for ethanol's use in ethylene glycol poisoning?

Accepted Answer

Competitive inhibitor of alcohol dehydrogenase

Answer

Competitive inhibitor of NADPH oxidase

Answer

Competitive inhibitor of aldehyde dehydrogenase

Answer

Non-competitive inhibitor of aldehyde dehydrogenase

Question 7

Which one of the following drugs cannot cause Pseudotumor Cerebri ?

Accepted Answer

Metformin

Answer

Nitrofurantoin

Answer

Tetracycline

Answer

Nalidixic acid

Question 8

All of the following are adverse effects of thalidomide except:

Accepted Answer

Myocarditis

Answer

Constipation

Answer

Peripheral neuropathy

Answer

Sedation

Question 9

Adverse reactions following whole-cell pertussis immunization include:

Accepted Answer

All of the options

Answer

Fever

Answer

Anaphylaxis

Answer

Local swelling

Question 10

The Drug of choice for a pregnant woman in 2nd trimester with pustular psoriasis is:

Accepted Answer

Prednisolone

Answer

Acitretin

Answer

Methotrexate

Answer

Dapsone

Clinical Pharmacology and Drug Toxicity — MCQs

Clinical Pharmacology and Drug Toxicity — MCQs

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