Drug Interactions Practice Questions

Q: A patient with glaucoma and bronchial asthma presents with status asthmaticus. What causative agent might have precipitated this condition?

Timolol eye drop. **Explanation:** **1. Why Timolol is the Correct Answer:** Timolol is a **non-selective beta-blocker** ($\beta_1$ and $\beta_2$ antagonist) commonly used as first-line therapy for glaucoma to decrease aqueous humor production. Even when administered topically as eye drops, significant systemic absorption occurs via the nasolacrimal duct, bypassing first-pass metabolism. In patients with pre-existing bronchial asthma, the blockade of $\beta_2$ receptors in the bronchial smooth muscle leads to bronchoconstriction, which can precipitate life-threatening **status asthmaticus**. **2. Analysis of Incorrect Options:** * **Pilocarpine (Option A):** A direct-acting cholinergic agonist (miotic). While it can cause bronchoconstriction in theory, it is not a beta-blocker and is rarely associated with precipitating status asthmaticus compared to $\beta$-blockers. * **Betaxolol (Option C):** This is a **cardioselective ($\beta_1$) blocker**. Because it lacks significant $\beta_2$ antagonist activity, it is the safest beta-blocker for glaucoma patients who also have respiratory diseases (though it should still be used with caution). * **Levobunolol (Option D):** Like timolol, it is a non-selective beta-blocker. However, Timolol is the classic prototype and the most frequently cited agent in exam questions regarding this specific adverse interaction. **3. NEET-PG High-Yield Pearls:** * **Systemic Absorption:** To minimize systemic side effects of eye drops, patients should be taught **nasolacrimal occlusion** (pressing the inner canthus) for 1–2 minutes after instillation. * **Drug of Choice:** For a glaucoma patient with asthma, **Betaxolol** is the preferred beta-blocker, or alternative classes like Prostaglandin analogues (Latanoprost) should be used. * **Contraindications for Timolol:** Asthma, COPD, Bradycardia, and Second/Third-degree heart block.

Q: Theophylline levels in blood are increased by which of the following?

Cimetidine. ### Explanation Theophylline is a methylxanthine with a **narrow therapeutic index**, meaning small changes in its serum concentration can lead to toxicity (seizures, arrhythmias). It is primarily metabolized in the liver by the **Cytochrome P450 (CYP1A2 and CYP3A4)** enzyme system. **1. Why Cimetidine is Correct:** Cimetidine is a potent **enzyme inhibitor**. It binds to the heme iron of the CYP450 system, reducing the metabolic clearance of theophylline. This leads to an increase in theophylline blood levels, significantly raising the risk of toxicity. **2. Why the Other Options are Incorrect:** * **Barbiturates (e.g., Phenobarbitone):** These are classic **enzyme inducers**. They increase the synthesis of CYP450 enzymes, thereby accelerating the metabolism of theophylline and **decreasing** its blood levels. * **Methotrexate:** While methotrexate has many drug interactions (especially with NSAIDs), it does not significantly inhibit the specific CYP enzymes responsible for theophylline metabolism. Therefore, it does not typically cause a rise in theophylline levels. **Clinical Pearls for NEET-PG:** * **The "G-PACMAN" Mnemonic for Enzyme Inhibitors:** **G**rapefruit juice, **P**rotease inhibitors, **A**zoles, **C**imetidine, **M**acrolides (except Azithromycin), **A**miodarone, **N**on-DHP CCBs (Verapamil/Diltiazem). These all can increase levels of drugs like theophylline, warfarin, and phenytoin. * **Smoking Effect:** Cigarette smoking **induces CYP1A2**, which *decreases* theophylline levels. If a patient stops smoking abruptly while on theophylline, their blood levels may rise to toxic levels. * **Alternative H2 Blocker:** If an H2 blocker is needed for a patient on theophylline, **Famotidine** or **Ranitidine** are preferred as they have minimal inhibitory effects on CYP450 compared to Cimetidine.

Q: Tacrolimus level is increased by all of the following drugs except?

Rifampicin. **Explanation:** The core concept behind this question is the **Cytochrome P450 (CYP3A4) enzyme system**. Tacrolimus, a potent calcineurin inhibitor used in organ transplantation, is primarily metabolized by the CYP3A4 isoenzyme in the liver and intestines. **1. Why Rifampicin is the correct answer:** Rifampicin is a classic, potent **enzyme inducer**. It increases the synthesis and activity of CYP3A4 enzymes. When co-administered with Tacrolimus, Rifampicin accelerates its metabolism, leading to **decreased** plasma levels of Tacrolimus. This can result in sub-therapeutic drug concentrations and an increased risk of graft rejection. **2. Why the other options are incorrect:** Options A, B, and C are all **enzyme inhibitors**: * **Erythromycin (Macrolide):** A well-known inhibitor of CYP3A4. * **Itraconazole (Azole antifungal):** One of the most potent inhibitors of the CYP3A4 system. * **Danazol (Androgen):** Also acts as a CYP3A4 inhibitor. These drugs decrease the metabolism of Tacrolimus, thereby **increasing** its serum concentration and increasing the risk of toxicity (e.g., nephrotoxicity, neurotoxicity). **Clinical Pearls & High-Yield Facts for NEET-PG:** * **The "Big" Inducers (Decrease Tacrolimus levels):** Rifampicin, Phenytoin, Carbamazepine, Phenobarbitone, and St. John’s Wort. * **The "Big" Inhibitors (Increase Tacrolimus levels):** Ketoconazole/Itraconazole, Erythromycin/Clarithromycin, Verapamil/Diltiazem, and **Grapefruit juice**. * **Monitoring:** Because Tacrolimus has a narrow therapeutic index, Therapeutic Drug Monitoring (TDM) is mandatory when starting or stopping any of the above medications. * **Cyclosporine** follows the same metabolic pathway and interaction profile as Tacrolimus.

Q: All of the following drugs can precipitate Tacrolimus toxicity, except:

Rifampicin. **Explanation:** The core concept in this question involves distinguishing between **pharmacokinetic** and **pharmacodynamic** drug interactions. **Why Rifampicin is the correct answer:** Tacrolimus is a calcineurin inhibitor primarily metabolized by the hepatic enzyme **CYP3A4**. **Rifampicin** is a potent **CYP450 inducer**. When co-administered, Rifampicin accelerates the metabolism of Tacrolimus, leading to *decreased* plasma levels and potential graft rejection, rather than toxicity. To cause toxicity, a drug would need to be a CYP3A4 inhibitor (e.g., Ketoconazole, Erythromycin, or Grapefruit juice). **Why the other options are incorrect:** Options A, B, and C (Gentamicin, Cisplatin, and Vancomycin) do not necessarily increase the blood concentration of Tacrolimus, but they precipitate toxicity through **additive pharmacodynamic effects**. * **Tacrolimus** is inherently **nephrotoxic** (causing afferent arteriolar vasoconstriction). * **Gentamicin (Aminoglycoside)**, **Cisplatin**, and **Vancomycin** are also well-known nephrotoxins. * Co-administration of these agents with Tacrolimus significantly increases the risk of acute kidney injury (AKI), thereby "precipitating" clinical toxicity. **High-Yield Clinical Pearls for NEET-PG:** * **Tacrolimus Toxicity Profile:** Nephrotoxicity (most common), Neurotoxicity (tremors, seizures), and New-onset Diabetes After Transplantation (NODAT). * **Drug of Choice:** Tacrolimus is preferred over Cyclosporine because it has a lower incidence of hirsutism and gum hyperplasia. * **Monitoring:** Therapeutic Drug Monitoring (TDM) is mandatory for Tacrolimus due to its narrow therapeutic index. * **Rule of Thumb:** Enzyme *Inducers* (Rifampicin, Phenytoin, Carbamazepine) decrease levels; Enzyme *Inhibitors* (Macrolides, Azoles) increase levels.

Q: Oral contraceptives are not given with which of the following medications?

Grisiofulvin. **Explanation:** The correct answer is **Griseofulvin**. **1. Why Griseofulvin is correct:** Oral contraceptive pills (OCPs) are primarily metabolized in the liver by the **Cytochrome P450 (CYP450)** enzyme system. Griseofulvin is a potent **microsomal enzyme inducer**. When co-administered, it increases the rate of metabolism of estrogen and progesterone components of the OCP, leading to decreased plasma concentrations of these hormones. This results in **contraceptive failure** and an increased risk of unintended pregnancy. **2. Why other options are incorrect:** * **Streptomycin:** This is an aminoglycoside that is not metabolized by the liver and does not induce or inhibit CYP450 enzymes. * **Pyrazinamide and Ethambutol:** These are first-line antitubercular drugs. Unlike Rifampicin (which is a powerful enzyme inducer and a classic cause of OCP failure), Pyrazinamide and Ethambutol do not significantly affect the hepatic metabolism of other drugs. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **The "Rifampicin Rule":** Among antitubercular drugs, **Rifampicin** is the most notorious enzyme inducer causing OCP failure. * **Other Enzyme Inducers (Mnemonic: GPRS Cell Phone):** **G**riseofulvin, **P**henytoin, **R**ifampicin, **S**moking, **C**arbamazepine, **P**henobarbitone. All these can decrease OCP efficacy. * **Antibiotic Interaction:** Broad-spectrum antibiotics (like Ampicillin or Tetracycline) were traditionally thought to decrease OCP efficacy by interfering with **enterohepatic circulation** (killing gut flora that deconjugate estrogens), though clinical evidence for this is less robust than for enzyme inducers. * **Management:** Patients on enzyme-inducing drugs should be advised to use an alternative or additional method of contraception (e.g., barrier methods).

Q: Which of the following drugs interacts with cefotaxime?

Loop diuretics. ### Explanation **Correct Option: C. Loop diuretics** The interaction between **Cefotaxime** (a 3rd generation cephalosporin) and **Loop diuretics** (like Furosemide) is a classic example of additive **nephrotoxicity**. **Mechanism:** While cephalosporins are generally safe, they are primarily excreted via the kidneys. Loop diuretics can cause dehydration and reduce renal blood flow, which decreases the clearance of cephalosporins [2]. This leads to higher concentrations of the antibiotic in the renal tubules, increasing the risk of acute tubular necrosis. This interaction is particularly significant in elderly patients or those with pre-existing renal impairment [1]. **Analysis of Incorrect Options:** * **A. Digoxin:** Digoxin primarily interacts with drugs that affect potassium levels (like diuretics) [2] or P-glycoprotein inhibitors (like Verapamil/Amiodarone). It does not have a clinically significant interaction with cefotaxime. * **B. Paracetamol:** This is a safe analgesic/antipyretic frequently co-administered with antibiotics. There is no documented pharmacokinetic or pharmacodynamic interaction between the two. * **D. Nifedipine:** As a Calcium Channel Blocker, its interactions usually involve CYP3A4 inhibitors/inducers. It does not interfere with the renal excretion or toxicity profile of cefotaxime. **High-Yield Clinical Pearls for NEET-PG:** * **Cephalosporin + Aminoglycosides:** This combination also significantly increases the risk of nephrotoxicity. * **Disulfiram-like Reaction:** Remember that certain cephalosporins (Cefoperazone, Cefotetan) contain a **Methylthiotetrazole (MTT) side chain** which causes a reaction with alcohol. * **Probenecid Interaction:** Probenecid inhibits the renal tubular secretion of most cephalosporins, leading to increased and prolonged plasma levels (often used therapeutically to extend drug action).

Question 1

A patient with glaucoma and bronchial asthma presents with status asthmaticus. What causative agent might have precipitated this condition?

Accepted Answer

Timolol eye drop

Answer

Pilocarpine eye drop

Answer

Betaxolol eye drop

Answer

Levobunolol eye drop

Question 2

Theophylline levels in blood are increased by which of the following?

Accepted Answer

Cimetidine

Answer

Barbiturates

Answer

Methotrexate

Answer

All of the above

Question 3

Probenecid interacts with which of the following antibiotics?

Accepted Answer

Ampicillin

Answer

Streptomycin

Answer

Vancomycin

Answer

Erythromycin

Question 4

Tacrolimus level is increased by all of the following drugs except?

Accepted Answer

Rifampicin

Answer

Erythromycin

Answer

Itraconazole

Answer

Danazol

Question 5

All of the following drugs can precipitate Tacrolimus toxicity, except:

Accepted Answer

Rifampicin

Answer

Gentamicin

Answer

Cisplatin

Answer

Vancomycin

Question 6

A 60-year-old patient with chronic liver disease and rheumatoid arthritis is to be treated with procainamide. He is already taking digoxin, hydrochlorothiazide, and potassium supplementation. Which of the following statements is relevant to this patient's treatment?

Accepted Answer

Hyperkalemia should be avoided to reduce the likelihood of procainamide toxicity.

Answer

A possible drug interaction with digoxin suggests that digoxin blood levels should be obtained before and after starting procainamide.

Answer

Procainamide cannot be used if the patient has asthma because it has a beta-blocking effect.

Answer

Procainamide is not active by the oral route.

Question 7

Antiepileptic effect of phenytoin is increased by all of the following except:

Accepted Answer

Sucralfate

Answer

Isoniazid

Answer

Cimetidine

Answer

Warfarin

Question 8

Oral contraceptive pills fail when used with the following drugs, EXCEPT:

Accepted Answer

Aspirin

Answer

Phenytoin

Answer

Rifampin

Answer

Tetracycline

Question 9

Oral contraceptives are not given with which of the following medications?

Accepted Answer

Grisiofulvin

Answer

Streptomycin

Answer

Pyraziniamide

Answer

Ethambutol

Question 10

Which of the following drugs interacts with cefotaxime?

Accepted Answer

Loop diuretics

Answer

Digoxin

Answer

Paracetamol

Answer

Nifedipine

Drug Interactions — MCQs

Drug Interactions — MCQs

On this page

Practice by Chapter

Want unlimited practice?