Clinical Pharmacology and Drug Toxicity — MCQs

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

Question 731: 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 732: Drug causing oliguria through prostaglandin inhibition is:

A. Aspirin (Correct Answer)
B. Montelukast
C. Diazepam
D. Acyclovir

Explanation: ***Aspirin*** - **Aspirin** and other **NSAIDs** cause oliguria by **inhibiting cyclooxygenase (COX)**, which reduces prostaglandin synthesis - Prostaglandins (especially PGE2 and PGI2) normally maintain renal vasodilation and adequate glomerular filtration - **Inhibition leads to**: Afferent arteriolar vasoconstriction → ↓ Renal blood flow → ↓ GFR → **Oliguria** - **High-risk patients**: Pre-existing renal disease, heart failure, volume depletion, elderly - This is a **hemodynamic/functional** renal impairment *Montelukast* - **Leukotriene receptor antagonist** used for asthma and allergic rhinitis - Acts on airways, not kidneys - No significant association with oliguria or renal dysfunction *Diazepam* - **Benzodiazepine** acting on CNS GABA receptors - Used for anxiety, seizures, muscle relaxation - No direct renal effects or oliguria association *Acyclovir* - **Antiviral drug** that can cause nephrotoxicity via **crystal formation** in renal tubules (crystal nephropathy) - Can lead to acute kidney injury and oliguria, especially with rapid IV infusion or dehydration - However, mechanism is **direct tubular toxicity**, NOT prostaglandin inhibition - The question specifically asks for prostaglandin-mediated oliguria, making **Aspirin** the correct answer

Question 733: A drug used in acute gout -

A. Colchicine (Correct Answer)
B. Sulfinpyrazone
C. Allopurinol
D. Probenecid

Explanation: ***Colchicine*** - **Colchicine** is an anti-inflammatory drug that is effective in treating acute gout flares by inhibiting neutrophil migration and activation. - It is often used as a first-line treatment for acute gout, particularly in its early stages. *Sulfinpyrazone* - **Sulfinpyrazone** is a uricosuric agent, meaning it increases the excretion of uric acid via the kidneys. - It is used for **long-term management** of chronic gout, not for acute attacks. *Probenecid* - **Probenecid** is also a uricosuric drug that works by inhibiting the reabsorption of uric acid in the renal tubules. - Like sulfinpyrazone, it is used for **prophylaxis** in chronic gout to lower serum uric acid levels, not for an acute flare. *Allopurinol* - **Allopurinol** is a xanthine oxidase inhibitor, which reduces the production of uric acid in the body. - It is a cornerstone of **chronic gout management** to prevent future attacks but is not indicated for the immediate treatment of an acute flare as it can sometimes worsen the acute attack initially.

Question 734: Lead absorbed by inhalation in the body is mainly eliminated through:

A. Sweat
B. Stool
C. Urine (Correct Answer)
D. None of the options

Explanation: ***Urine*** - Lead is primarily eliminated from the body via **renal excretion**, with approximately **65-75% of absorbed lead** being excreted through the kidneys. - This process involves **glomerular filtration** and **tubular secretion**, making urinary excretion the **major pathway** for lead elimination in both acute and chronic exposure. - Urinary lead levels are commonly used as a biomarker of recent lead exposure. *Stool* - Fecal elimination accounts for approximately **15-25% of absorbed lead**, making it the **second most important route** of elimination. - This occurs through **biliary excretion** and direct intestinal secretion into the gastrointestinal tract. - While significant, it remains a **secondary pathway** compared to renal excretion. *Sweat* - Lead excretion through sweat represents a **minor pathway** accounting for less than 1% of total elimination. - The amount of lead lost through perspiration is generally **insignificant** compared to renal and fecal routes. *None of the options* - This is incorrect because **urine is definitively the primary route** for lead elimination from the body. - Multiple elimination pathways exist, with urinary excretion being the most important.

Question 735: Na content (mEq/L) in Normal saline is:

A. 135
B. 130
C. 154 (Correct Answer)
D. 111

Explanation: ***154*** - Normal saline, or 0.9% sodium chloride, contains **154 mEq/L of sodium (Na+)** and 154 mEq/L of chloride (Cl-). - This concentration is nearly **isotonic** with plasma, making it a common intravenous fluid for volume repletion. *135* - This value is close to the lower end of the normal range for **serum sodium concentration** (typically 135-145 mEq/L) in the human body. - It does not represent the sodium content of normal saline solution. *130* - This sodium concentration is **hypotonic** relative to normal plasma. - It is not the standard sodium content found in 0.9% normal saline. *111* - This value is significantly **hypotonic** and would indicate hyponatremia if it were a serum sodium level. - It is much lower than the sodium content of normal saline.

Question 736: All of the following can cause SLE-like syndrome except

A. Isoniazid
B. Hydralazine
C. Penicillin (Correct Answer)
D. Sulphonamide

Explanation: ***Penicillin*** - Penicillin is known to cause **drug-induced hemolytic anemia**, **allergic reactions**, and **serum sickness-like reactions**, but not typically an SLE-like syndrome. - While it can induce certain autoimmune phenomena, it does not commonly trigger the specific constellation of symptoms and autoantibodies associated with drug-induced lupus. *Isoniazid* - **Isoniazid** is a well-known cause of **drug-induced lupus erythematosus**, particularly in slow acetylators. - It can lead to positive **antinuclear antibodies (ANAs)** and clinical symptoms mimicking SLE. *Hydralazine* - **Hydralazine** is a classic drug associated with **drug-induced lupus**, often presenting with **arthralgias**, **myalgias**, and **fever**. - It commonly induces **anti-histone antibodies** and **ANA** without significant renal or central nervous system involvement. *Sulphonamide* - **Sulfonamides** (such as sulfasalazine) can induce an **SLE-like syndrome** and are recognized causes of drug-induced lupus. - They are associated with the development of **autoantibodies** and systemic symptoms similar to spontaneous SLE.

Question 737: A 30-year-old highly health conscious woman has been ingesting vitamins and health foods. She is complaining of hair loss, double vision and headache. Her liver function tests are abnormal. She may be suffering from

A. Vitamin E deficiency
B. Hypervitaminosis D
C. Hypervitaminosis A (Correct Answer)
D. Vitamin C deficiency

Explanation: ***Hypervitaminosis A*** - Chronic intake of excessive amounts of **vitamin A** can lead to symptoms such as **hair loss**, **double vision (diplopia)**, and **headache**. - **Liver function abnormalities** are a common feature of hypervitaminosis A due to the liver's role in vitamin A storage and metabolism. *vitamin E deficiency* - **Vitamin E deficiency** typically manifests with neurological symptoms like **ataxia**, **peripheral neuropathy**, and **muscle weakness**, given its role as an antioxidant. - It is not associated with the constellation of symptoms presented, especially **hair loss**, **double vision**, **headache**, and **liver dysfunction**. *Hypervitaminosis D* - **Hypervitaminosis D** primarily leads to **hypercalcemia**, presenting with symptoms such as **nausea**, **vomiting**, **polyuria**, and **kidney stones**. - It does not typically cause **hair loss**, **double vision**, or direct effects on **liver function** in the way described. *Vitamin C deficiency* - **Vitamin C deficiency** (scurvy) is characterized by symptoms like **gingival bleeding**, **petechiae**, **poor wound healing**, and **fatigue**. - These symptoms are distinctly different from the **neurological and hepatic manifestations** seen in the patient.

Question 738: Which of the following drugs shows nephrotoxicity during administration?

A. Azathioprine
B. Tacrolimus (Correct Answer)
C. Mycophenolate mofetil
D. Leflunomide

Explanation: ***Tacrolimus*** - **Tacrolimus** is a calcineurin inhibitor and a well-known cause of **nephrotoxicity**, which can manifest as acute kidney injury or chronic renal dysfunction [1], [4]. - Its mechanism involves vasoconstriction of afferent arterioles and direct tubular toxicity, leading to reduced glomerular filtration. *Azathioprine* - **Azathioprine** is an immunosuppressant primarily associated with **bone marrow suppression** (leukopenia, thrombocytopenia) and **hepatotoxicity**, not typically nephrotoxicity [2]. - While it can cause renal impairment in rare cases, it is not a primary mechanism of action. *Mycophenolate mofetil* - **Mycophenolate mofetil (MMF)** is an immunosuppressant that primarily causes **gastrointestinal side effects** (diarrhea, nausea) and **myelosuppression**. - It is generally considered **renal-sparing** and is often used in situations where calcineurin inhibitors are contraindicated due to nephrotoxicity. *Leflunomide* - **Leflunomide** is an immunosuppressant used in rheumatoid arthritis, known for causing **hepatotoxicity**, **hypertension**, and **teratogenicity** [3]. - While it can affect various organ systems, direct and significant nephrotoxicity is not a prominent adverse effect.

Question 739: The drug that can cause hirsutism is

A. Dactinomycin
B. Cycloserine
C. Minoxidil (Correct Answer)
D. Valsartan

Explanation: ***Minoxidil*** - **Minoxidil** is a potent **vasodilator** that can cause **hirsutism** as a common side effect, especially when used orally. - Due to its hair growth stimulating effect, it is also topically used to treat **androgenetic alopecia** [1]. *Dactinomycin* - **Dactinomycin** is an **antineoplastic antibiotic** primarily used in cancer chemotherapy. - Its main side effects include **myelosuppression**, nausea, vomiting, and mucositis, not hirsutism. *Cycloserine* - **Cycloserine** is an antibiotic mainly used to treat **tuberculosis** [2]. - Its adverse effects are predominantly **neurological** and psychiatric, such as seizures and psychosis, not affecting hair growth [2]. *Valsartan* - **Valsartan** is an **angiotensin receptor blocker (ARB)** used to treat hypertension and heart failure. - Common side effects include dizziness and hyperkalemia; it does not cause hirsutism.

Question 740: About Vi polysaccharide vaccine, true is:

A. Can be given in patients with yellow fever and hepatitis B (Correct Answer)
B. Has many serious local side effects
C. Has many serious systemic side effects
D. Has many contraindications

Explanation: ***Can be given in patients with yellow fever and hepatitis B*** - There are **no contraindications** for administering the **Vi polysaccharide vaccine** to individuals with **yellow fever** or **hepatitis B**. These conditions do not interfere with the vaccine's safety or efficacy. - The Vi polysaccharide vaccine is specifically designed to protect against **typhoid fever** and is generally safe, even in immunocompromised individuals or those with concurrent infections. *Has many serious local side effects* - The **Vi polysaccharide vaccine** is known for its **mild local side effects**, typically limited to pain, redness, or swelling at the injection site. - **Serious local reactions** are **rare** and not a characteristic feature of this vaccine. *Has many serious systemic side effects* - The **Vi polysaccharide vaccine** generally has a **good safety profile** with **few systemic side effects**. - Systemic reactions, if they occur, are usually mild and transient, such as low-grade fever or headache, rather than serious. *Has many contraindications* - The **Vi polysaccharide vaccine** has **few contraindications**. The main contraindication is a **severe allergic reaction** to a previous dose or any vaccine component. - It is safe for use in most populations, including individuals with chronic diseases, and does not have a large list of conditions that would prevent its administration.

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Principles of Clinical Pharmacology

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Drug-Induced Liver Injury

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Drug-Induced Blood Dyscrasias

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