Drug Interactions — MCQs

Drug Interactions Indian Medical PG Practice Questions and MCQs

Question 141: Spironolactone should be used with extreme caution or avoided with which of the following drugs?

A. ACE inhibitor (e.g., Enalapril) (Correct Answer)
B. Beta-blocker (e.g., Atenolol)
C. Thiazide diuretic (e.g., Chlorthiazide)
D. Calcium channel blocker (e.g., Verapamil)

Explanation: ***ACE inhibitor (e.g., Enalapril)*** - The combination of **spironolactone**, a **potassium-sparing diuretic**, and an **ACE inhibitor** significantly increases the risk of **hyperkalemia** due to their synergistic effects on potassium retention. - Both drug classes reduce **aldosterone activity** and lead to decreased potassium excretion, potentially causing life-threatening cardiac arrhythmias. *Beta-blocker (e.g., Atenolol)* - While beta-blockers can affect potassium levels, the risk of severe **hyperkalemia** when combined with **spironolactone** is usually manageable and does not represent a direct contraindication. - This combination is often used in managing conditions like **heart failure**, with careful monitoring. *Thiazide diuretic (e.g., Chlorthiazide)* - **Thiazide diuretics** tend to cause **hypokalemia**, and spironolactone can be used in combination to **counteract** this potassium loss. - This combination is often beneficial, as spironolactone helps to conserve potassium while the thiazide diuretic promotes diuresis, reducing the overall risk of electrolyte imbalance. *Calcium channel blocker (e.g., Verapamil)* - Calcium channel blockers primarily affect **calcium influx** into cells and have no direct significant interaction with spironolactone regarding potassium levels. - There is no contraindication for combining these two drug classes, and they are frequently used together safely for various cardiovascular conditions.

Question 142: Severe hyperkalemia is seen in combination with:

A. Amiloride and Furosemide
B. Lisinopril and Furosemide
C. Losartan and amiloride (Correct Answer)
D. Propranolol and verapamil

Explanation: ***Losartan and amiloride*** - **Losartan** is an **angiotensin receptor blocker (ARB)**, often leading to **hyperkalemia** by inhibiting aldosterone secretion. - **Amiloride** is a **potassium-sparing diuretic**, directly interfering with sodium reabsorption and potassium excretion in the **collecting duct**. The combination of Na⁺-channel inhibitors like amiloride with angiotensin-converting enzyme inhibitors (or ARBs) carries a risk of life-threatening hyperkalemia [1].*Amiloride and Furosemide* - **Furosemide** is a **loop diuretic** that causes **potassium wasting**, thus counteracting the potassium-sparing effect of amiloride [2]. - Combining these two drugs typically results in a **neutral or mildly hypokalemic effect**, not severe hyperkalemia.*Lisinopril and furosemide* - **Lisinopril** is an **ACE inhibitor** that causes **hyperkalemia** by reducing aldosterone levels. - However, **furosemide** induces **hypokalemia**, significantly mitigating the hyperkalemic potential of lisinopril [2].*Propranolol and verapamil* - **Propranolol** (a beta-blocker) and **verapamil** (a calcium channel blocker) primarily affect heart rate and contractility, and blood pressure. - Neither of these drugs is directly associated with significant alterations in **potassium levels** to cause severe hyperkalemia.

Question 143: Which antibiotic potentiates the effect of neuromuscular blockers?

A. Erythromycin
B. Aminoglycoside (Correct Answer)
C. Nitrofurantoin
D. Co-trimoxazole

Explanation: ***Aminoglycoside*** - **Aminoglycosides** inhibit presynaptic release of **acetylcholine** and suppress postsynaptic sensitivity to acetylcholine, thereby enhancing the effects of **neuromuscular blockers (NMBs)**. - This potentiation can lead to prolonged **neuromuscular blockade** and **respiratory depression**, especially in patients with impaired renal function or pre-existing neuromuscular disease. *Erythromycin* - **Erythromycin**, a **macrolide antibiotic**, is primarily known for inhibiting the **cytochrome P450 3A4 (CYP3A4)** enzyme, which can alter the metabolism of many drugs. - It does not directly impact **acetylcholine** release or receptor sensitivity to the extent that it significantly potentiates **neuromuscular blockers**. *Nitrofurantoin* - **Nitrofurantoin** is an **antibiotic** used predominantly for **urinary tract infections** and acts by damaging bacterial DNA and ribosomal proteins. - There is no known significant interaction or potentiation effect of **nitrofurantoin** on **neuromuscular blockers**. *Co-trimoxazole* - **Co-trimoxazole (trimethoprim-sulfamethoxazole)** is a combination **antibiotic** that interferes with bacterial **folic acid synthesis**. - It does not interfere with **neuromuscular transmission** or potentiate **neuromuscular blockers**, unlike aminoglycosides.

Question 144: A lady gets pregnant even though she was on contraceptive pills. She is suspected to have consumed

A. Ciprofloxacin
B. Rifampicin (Correct Answer)
C. Streptomycin
D. None of these

Explanation: ***Rifampicin*** - **Rifampicin** is a potent inducer of **hepatic microsomal enzymes** (cytochrome P450 enzymes), particularly CYP3A4. - This enzyme induction leads to increased metabolism and thus decreased effectiveness of **oral contraceptive pills**, raising the risk of unintended pregnancy. *Ciprofloxacin* - **Ciprofloxacin** is a **quinolone antibiotic** that primarily works by inhibiting bacterial DNA gyrase and topoisomerase IV. - It does not significantly induce hepatic enzymes or interfere with the efficacy of **oral contraceptive pills**. *Streptomycin* - **Streptomycin** is an **aminoglycoside antibiotic** that inhibits bacterial protein synthesis. - It is not known to have a significant drug interaction with **oral contraceptive pills** that would lead to contraceptive failure. *None of these* - This option is incorrect because **Rifampicin** is well-documented to reduce the effectiveness of **oral contraceptive pills**.

Question 145: Cilastatin is given in combination with Imipenem because:-

A. Inhibits the enzymes that digest Imipenem in stomach
B. Cilastatin prevents degradation of Imipenem in kidney (Correct Answer)
C. Reduces side effects of Imipenem
D. Cilastatin increases absorption of Imipenem

Explanation: ***Cilastatin prevents degradation of Imipenem in kidney*** - **Imipenem** is extensively metabolized in the renal tubules by the enzyme **dihydropeptidase-I**, leading to its inactivation and potential nephrotoxicity. - **Cilastatin** is a **dihydropeptidase-I inhibitor** that prevents this enzymatic breakdown, increasing the bioavailability and efficacy of imipenem and reducing the risk of renal damage. *Inhibits the enzymes that digest Imipenem in stomach* - **Imipenem** is a parenteral antibiotic and is not administered orally; therefore, degradation in the stomach is not a relevant concern. - Its combination with cilastatin is specifically to address renal metabolism, not gastric degradation. *Cilastatin increase absorption of Imipenem* - **Cilastatin** does not enhance the absorption of imipenem; its role is primarily to inhibit renal metabolism. - Imipenem is administered intravenously, bypassing the need for gastrointestinal absorption. *Reduces side effects of Imipenem* - While cilastatin does prevent the formation of nephrotoxic metabolites of imipenem, its primary role is to **maintain therapeutic levels** and prevent drug inactivation. - The reduction in **nephrotoxicity** is a consequence of preventing degradation, rather than a direct mitigation of general side effects.

Question 146: A patient is on warfarin therapy. All of the following drugs increase the risk of bleeding with warfarin except?

A. Isoniazid
B. Amiodarone
C. Carbamazepine (Correct Answer)
D. Cimetidine

Explanation: ***Carbamazepine*** - Carbamazepine **induces cytochrome P450 enzymes**, specifically **CYP3A4** and **CYP2C9**, which are responsible for warfarin metabolism. - This induction leads to a **faster metabolism of warfarin**, thus **decreasing its anticoagulant effect** and thereby reducing the risk of bleeding. *Isoniazid* - Isoniazid is an **inhibitor of cytochrome P450 enzymes**, primarily **CYP2C9**, which metabolizes the more potent S-warfarin isomer. - This inhibition **decreases warfarin metabolism**, leading to **increased anticoagulant effect** and higher risk of bleeding. *Amiodarone* - Amiodarone is a potent **inhibitor of cytochrome P450 enzymes**, significantly **CYP2C9** and **CYP3A4**. - It leads to a **reduced metabolism of warfarin**, causing **elevated INR** and an increased risk of bleeding. *Cimetidine* - Cimetidine is a known **inhibitor of various cytochrome P450 enzymes**, particularly **CYP1A2**, **CYP2C9**, and **CYP3A4**. - Its inhibitory action on warfarin metabolism results in **higher warfarin levels** and an **increased risk of bleeding**.

Question 147: A 75-year-old male on warfarin is prescribed an antibiotic for pneumonia. Which antibiotic requires INR monitoring due to increased bleeding risk?

A. Ciprofloxacin (Correct Answer)
B. Amoxicillin
C. Clindamycin
D. Azithromycin

Explanation: ***Ciprofloxacin*** - **Ciprofloxacin** and other fluoroquinolones can interact with **warfarin**, though the mechanism is **not well-established** and likely multifactorial (may involve gut flora disruption, protein binding displacement, or metabolic effects). - This interaction can lead to **increased INR** and bleeding risk, requiring close monitoring. - Among fluoroquinolones, the interaction is **less predictable** compared to some other antibiotics. *Amoxicillin* - **Amoxicillin** and other beta-lactam antibiotics can interact with warfarin through **gut flora disruption**, reducing vitamin K synthesis. - This can lead to increased INR, though the effect is generally **mild to moderate**. - Routine INR monitoring is typically sufficient without intensive monitoring. *Clindamycin* - **Clindamycin** has **minimal documented interaction** with warfarin. - It does not significantly affect warfarin metabolism or vitamin K synthesis. - Generally considered a **safer option** for patients on warfarin therapy. *Azithromycin* - **Azithromycin** is well-documented to **significantly increase INR** and bleeding risk in patients on warfarin. - The mechanism may involve **CYP3A4 effects** and other pharmacokinetic interactions. - **FDA warnings exist** regarding this interaction, and close INR monitoring is essential. - Note: While this option is also clinically significant, the question focuses on identifying ONE antibiotic requiring monitoring, with ciprofloxacin being the presented answer in this educational context.

Question 148: A patient on rifampin for TB starts birth control pills. What adjustment is needed?

A. Add a second hormonal contraceptive
B. Switch to non-hormonal contraception (Correct Answer)
C. Increase birth control dose
D. No change needed

Explanation: ***Switch to non-hormonal contraception*** - **Rifampin** is a potent **CYP450 enzyme inducer**, which significantly increases the metabolism of **estrogen and progestin** in birth control pills. - This interaction can lead to **reduced effectiveness** of oral contraceptives, increasing the risk of **unintended pregnancy**, making non-hormonal options more reliable. *Add a second hormonal contraceptive* - Adding another hormonal contraceptive in conjunction with the birth control pills would not circumvent the problem of **rifampin's enzyme-inducing effect** on hormonal metabolism. - This approach would still leave the patient at an **increased risk of contraceptive failure** due to rapid drug metabolism. *Increase birth control dose* - While increasing the dose might partially compensate for increased metabolism, the extent of **enzyme induction by rifampin** can be unpredictable and variable, making it difficult to find an effective and safe dose. - A higher dose of hormones can also lead to an **increased risk of side effects** such as **venous thromboembolism**. *No change needed* - This is incorrect because **rifampin significantly reduces the effectiveness of hormonal contraception** through enzyme induction. - Failing to make an adjustment would expose the patient to a **high risk of unintended pregnancy**.

Question 149: A 70-year-old patient with heart failure and low potassium is on digoxin and furosemide. Which medication addition could safely counteract hypokalemia without risking digoxin toxicity?

A. Amlodipine
B. Spironolactone (Correct Answer)
C. Calcium gluconate
D. Hydrochlorothiazide

Explanation: ***Spironolactone*** - **Spironolactone** is a **potassium-sparing diuretic** that helps counteract potassium loss caused by furosemide, thereby reducing the risk of **hypokalemia** - By preventing hypokalemia, spironolactone indirectly reduces the risk of **digoxin toxicity**, as hypokalemia potentiates the cardiac effects of digoxin and increases myocardial sensitivity to digoxin - This is the **standard of care** in heart failure patients on loop diuretics and digoxin *Amlodipine* - **Amlodipine** is a **calcium channel blocker** primarily used for **hypertension** and **angina** - It does not directly affect **potassium levels** and would not address the patient's hypokalemia - While safe with digoxin, it doesn't solve the underlying electrolyte problem *Calcium gluconate* - **Calcium gluconate** is primarily used to treat **hyperkalemia** or **hypocalcemia** - While it can be used to treat digoxin toxicity in emergency settings by stabilizing cardiac membranes, it does not prevent **hypokalemia** - It does not replenish potassium stores and is not appropriate for chronic management *Hydrochlorothiazide* - **Hydrochlorothiazide** is a **thiazide diuretic** that, like furosemide, causes **potassium wasting** through increased renal excretion - Adding it would **exacerbate** the patient's existing **hypokalemia**, significantly increasing the risk of **digoxin toxicity** - This combination would be potentially dangerous in this clinical scenario

Question 150: A patient on warfarin has a high INR. Which drug likely caused this?

A. Amiodarone (Correct Answer)
B. Phenytoin
C. Carbamazepine
D. Rifampicin

Explanation: ***Amiodarone*** - Amiodarone is a well-known inhibitor of **CYP2C9**, the primary enzyme responsible for the metabolism of **S-warfarin**, the more potent enantiomer of warfarin. - Inhibition of warfarin metabolism leads to increased warfarin levels, thereby enhancing its anticoagulant effect and causing a **higher INR**. *Phenytoin* - Phenytoin is an **enzyme inducer**, primarily of **CYP2C9** and **CYP3A4**. - Its interaction with warfarin typically leads to **decreased warfarin levels** and a **lower INR**, reducing the anticoagulant effect. *Carbamazepine* - Carbamazepine is a potent **enzyme inducer**, particularly of **CYP3A4** and **CYP2C9**. - Like phenytoin, it generally leads to **increased warfarin metabolism** and a **reduced INR**, thereby decreasing its anticoagulant efficacy. *Rifampicin* - Rifampicin is a strong **inducer of hepatic cytochrome P450 enzymes**, especially **CYP3A4** and **CYP2C9**. - Its co-administration with warfarin significantly **increases warfarin metabolism**, resulting in **lower warfarin concentrations** and a **decreased INR**.

Practice by Chapter

Mechanisms of Drug Interactions

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Pharmacokinetic Interactions

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Pharmacodynamic Interactions

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Drug-Food Interactions

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Drug-Disease Interactions

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Clinically Significant Drug Interactions

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Computer Systems for Detecting Drug Interactions

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Management of Drug Interactions

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Drug Interactions in Special Populations

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Role of P-glycoprotein in Drug Interactions

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