Rational Prescribing and Deprescribing — MCQs

10 questions

A patient given digoxin started having side effects like nausea and vomiting. The serum concentration of digoxin was 4 ng/mL. The plasma therapeutic range is 1-2 ng/mL. If the half-life of digoxin is 40 hours, how long should one wait before resuming the treatment?

A patient presents with nephrotic syndrome and hypoalbuminemia. Protein binding of which drug is not affected?

Acute allergic reaction to the penicillin group of drugs is classified as:

All of the following can cause SLE-like syndrome except

In which of the following clinical conditions does the use of anticoagulants provide maximum benefit?

Which of the following is true regarding prophylactic antibiotic use in surgical practice?

Which of these drugs can be given safely to a patient with renal disease?

Rivastigmine & donepezil are drugs used predominantly in the management of ?

Q10Medium

A diabetic female on Isoniazid (INH) and Rifampicin for tuberculosis developed Deep Vein Thrombosis (DVT). She was started on Warfarin, but her Prothrombin Time (PT) is not elevated. What is the next appropriate step in management?

Rational Prescribing and Deprescribing Indian Medical PG Practice Questions and MCQs

Question 1: A patient given digoxin started having side effects like nausea and vomiting. The serum concentration of digoxin was 4 ng/mL. The plasma therapeutic range is 1-2 ng/mL. If the half-life of digoxin is 40 hours, how long should one wait before resuming the treatment?

A. 120 hours
B. 140-180 hours
C. 1 half-life (40 hours)
D. 80 hours (Correct Answer)

Explanation: ***80 hours (2 half-lives)***- Current digoxin level is **4 ng/mL**, which is **twice the upper therapeutic limit** (2 ng/mL), causing toxicity with nausea and vomiting [1]- After **1 half-life (40 hours)**: concentration reduces to 2 ng/mL (upper therapeutic limit) [2]- After **2 half-lives (80 hours)**: concentration reduces to 1 ng/mL (mid-therapeutic range) [2]- **Clinical rationale**: While 2 ng/mL is technically within range, waiting for 2 half-lives ensures the level is comfortably in the **middle of the therapeutic window** (1 ng/mL), providing a **safer margin** before resuming treatment in a patient who just experienced toxicity- This conservative approach minimizes risk of recurrent toxicity, especially important given the patient's recent symptoms at 4 ng/mL*1 half-life (40 hours)*- After 1 half-life, digoxin level would be 2 ng/mL, which is at the **upper limit** of the therapeutic range- While technically within the therapeutic range, this leaves **minimal safety margin** in a patient who just experienced toxicity- Starting treatment immediately at this level carries higher risk of recurrent side effects*120 hours (3 half-lives)*- After 3 half-lives, the concentration would be **0.5 ng/mL**, which is **below the therapeutic range** (1-2 ng/mL)- This is overly conservative and would **unnecessarily delay** resumption of essential cardiac medication- Could lead to inadequate control of the underlying condition (heart failure or atrial fibrillation)*140-180 hours (3.5-4.5 half-lives)*- This would reduce digoxin to **0.25-0.35 ng/mL**, well below therapeutic levels- This **excessive delay** is not clinically justified and could worsen the patient's cardiac condition- No standard protocol recommends waiting this long before resuming digoxin therapy

Question 2: A patient presents with nephrotic syndrome and hypoalbuminemia. Protein binding of which drug is not affected?

A. Valproate
B. Morphine (Correct Answer)
C. Diazepam
D. Tolbutamide

Explanation: ***Morphine*** - Morphine is a **low protein-bound drug** (<35%), meaning a significant portion circulates freely. - Therefore, even with **reduced albumin levels** in nephrotic syndrome, the free fraction available for action is not significantly altered. *Valproate* - Valproate is **highly protein-bound** (90-95%), primarily to albumin. - In conditions like nephrotic syndrome with **hypoalbuminemia**, a decreased binding capacity leads to a higher free drug fraction and increased pharmacological effect. *Diazepam* - Diazepam is also **highly protein-bound** (98%), mainly to albumin. - Like other highly bound drugs, **hypoalbuminemia** in nephrotic syndrome would increase its free fraction, potentially leading to increased side effects. *Tolbutamide* - Tolbutamide is another drug with **high protein binding** (>90%), predominantly to albumin. - Reduced albumin levels in nephrotic syndrome would result in a **higher free concentration** of tolbutamide, increasing its hypoglycemic effect and risk of adverse reactions.

Question 3: Acute allergic reaction to the penicillin group of drugs is classified as:

A. Type 1 reaction (Correct Answer)
B. Type 2 reaction
C. Type 3 reaction
D. Type 4 reaction

Explanation: ***Type 1 reaction*** - Penicillin allergy is a classic example of a **Type I hypersensitivity reaction**, mediated by **IgE antibodies**. - Symptoms like **anaphylaxis**, **urticaria**, and **angioedema** develop rapidly upon re-exposure to the drug. *Type 2 reaction* - **Type II hypersensitivity reactions** involve **IgG** or **IgM antibodies** binding to antigens on cell surfaces, leading to cell destruction. - Examples include **hemolytic anemia** due to drug-induced antibodies, which is not the primary mechanism of typical penicillin allergy. *Type 3 reaction* - **Type III hypersensitivity reactions** involve the formation of **immune complexes** (antigen-antibody complexes) that deposit in tissues. - This can lead to conditions like **serum sickness** or **vasculitis**, which are less common manifestations of penicillin allergy. *Type 4 reaction* - **Type IV hypersensitivity reactions** are **delayed-type hypersensitivity (DTH)** reactions, mediated by **T cells** rather than antibodies. - These reactions typically manifest 24-72 hours after exposure, as seen in **contact dermatitis**; while some penicillin reactions can be T-cell mediated, the acute, life-threatening allergic response is Type I.

Question 4: 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 5: Match the following drugs in Column A with their contraindications in Column B. | Column A | Column B | | :-- | :-- | | 1. Morphine | 1. QT prolongation | | 2. Amiodarone | 2. Thromboembolism | | 3. Vigabatrin | 3. Pregnancy | | 4. Estrogen preparations | 4. Head injury |

A. A-1, B-3, C-2, D-4
B. A-4, B-1, C-3, D-2 (Correct Answer)
C. A-3, B-2, C-4, D-1
D. A-2, B-4, C-1, D-3

Explanation: ***A-4, B-1, C-3, D-2*** - **Morphine** is contraindicated in **head injury** as it can increase intracranial pressure and mask neurological symptoms. - **Amiodarone** is contraindicated in patients with **QT prolongation** due to its risk of inducing more severe arrhythmias like Torsades de Pointes. - **Vigabatrin** is contraindicated during **pregnancy** due to its potential for teratogenicity and adverse effects on fetal development. - **Estrogen preparations** are contraindicated in patients with a history of **thromboembolism** due to their increased risk of blood clot formation. *A-1, B-3, C-2, D-4* - This option incorrectly matches **Morphine** with QT prolongation and **Estrogen preparations** with head injury, which are not their primary contraindications. - It also incorrectly links **Vigabatrin** with thromboembolism and **Amiodarone** with pregnancy. *A-3, B-2, C-4, D-1* - This choice incorrectly associates **Morphine** with pregnancy and **Vigabatrin** with head injury, which are not the most critical or direct contraindications. - It also misaligns **Amiodarone** with thromboembolism and **Estrogen preparations** with QT prolongation. *A-2, B-4, C-1, D-3* - This option incorrectly matches **Morphine** with thromboembolism and **Amiodarone** with head injury, which are not their most significant contraindications. - It also incorrectly links **Vigabatrin** with QT prolongation and **Estrogen preparations** with pregnancy.

Question 6: In which of the following clinical conditions does the use of anticoagulants provide maximum benefit?

A. Prevention of recurrences of myocardial infarction
B. Prevention of venous thrombosis and pulmonary embolism (Correct Answer)
C. Prevention of cerebrovascular accident (stroke)
D. Retinal artery thrombosis

Explanation: ***Prevention of venous thrombosis and pulmonary embolism*** - Anticoagulants are highly effective in inhibiting the formation and extension of **venous thrombi**, thereby directly preventing **deep vein thrombosis (DVT)** and **pulmonary embolism (PE)**. - The mechanism of action targets the **coagulation cascade**, directly reducing the risk of these venous thromboembolic events, which are a major indication for anticoagulant therapy. *Prevention of recurrences of myocardial infarction* - While anticoagulants may play a secondary role, **antiplatelet agents** (e.g., aspirin, clopidogrel) are the primary therapy for preventing recurrent myocardial infarction, as **arterial thrombi** are predominantly platelet-rich. - Anticoagulants are used in specific high-risk situations post-MI (e.g., **atrial fibrillation**, left ventricular thrombus) but are not generally considered the primary preventive strategy. *Cerebrovascular accident* - The benefit of anticoagulants for stroke prevention is primarily significant in cases of **cardioembolic stroke** (e.g., due to **atrial fibrillation**) where they prevent clot formation in the heart. - For non-cardioembolic **ischemic strokes** (e.g., thrombotic or lacunar), antiplatelet agents are generally preferred for secondary prevention. *Retinal artery thrombosis* - **Retinal artery thrombosis** is often caused by **arterial atherosclerosis** and **embolism** from the carotid arteries or heart, where antiplatelet agents are typically primary. - The role of anticoagulants here is limited to specific causes like **atrial fibrillation** or in patients already on anticoagulation for other indications.

Question 7: Which of the following is true regarding prophylactic antibiotic use in surgical practice?

A. is given orally
B. continued for a minimum of 7 days
C. first dose is given before induction of anesthesia (Correct Answer)
D. depends on individual preference

Explanation: ***First dose is given before induction of anesthesia*** - **Prophylactic antibiotics** are most effective when present in adequate concentrations in tissue **before the surgical incision** is made - Administering the first dose **within 60 minutes before incision** (typically before induction of anesthesia) ensures optimal tissue levels at the time of potential bacterial contamination - This timing is a **key principle** of effective surgical antibiotic prophylaxis *Is given orally* - Surgical prophylaxis requires **intravenous administration** for rapid and reliable tissue levels - IV route ensures predictable bioavailability and adequate drug concentration at the surgical site - Oral route may be used in specific outpatient scenarios but is **not standard** for surgical prophylaxis *Continued for a minimum of 7 days* - Prophylactic antibiotics are given for **short duration**: typically a **single dose** or continued for less than 24 hours post-operatively - Extended courses (≥7 days) are reserved for **treating established infections**, not prophylaxis - Prolonged use increases risk of **antibiotic resistance**, adverse effects, and *Clostridioides difficile* infection *Depends on individual preference* - Prophylactic antibiotic use follows **evidence-based guidelines** and institutional protocols, not individual preference - Guidelines consider surgery type, patient risk factors, local **antibiogram data**, and established efficacy - Standardized protocols improve outcomes and reduce surgical site infections

Question 8: Which of these drugs can be given safely to a patient with renal disease?

A. Aminoglycoside
B. Phenacetin
C. Tetracycline
D. Morphine (Correct Answer)

Explanation: ***Morphine*** - Morphine is primarily metabolized in the **liver** and excreted as glucuronide conjugates, making it generally safer in patients with **renal impairment**. - While careful dosing and monitoring are still needed, its elimination is less dependent on **kidney function** compared to other drugs listed. *Phenacetin* - Phenacetin is an **NSAID** that is known to cause **analgesic nephropathy**, leading to chronic interstitial nephritis and papillary necrosis. - Its use is contraindicated in patients with existing **renal disease** due to the high risk of further kidney damage. *Tetracycline* - Tetracyclines can accumulate in patients with **renal impairment**, leading to increased side effects such as **nephrotoxicity** and increased **blood urea nitrogen (BUN)**. - Specifically, some tetracyclines (e.g., outdated tetracycline) can cause a **Fanconi-like syndrome** in susceptible individuals. *Aminoglycoside* - Aminoglycosides are extensively excreted by the kidneys and are highly **nephrotoxic**, causing acute tubular necrosis. - Their use in **renal disease** requires significant dose adjustments and careful monitoring of plasma levels to prevent further kidney damage and ototoxicity.

Question 9: Rivastigmine & donepezil are drugs used predominantly in the management of ?

A. Dissociation
B. Dementia (Correct Answer)
C. Delusions
D. Depression

Explanation: ***Dementia*** - **Rivastigmine** and **donepezil** are **acetylcholinesterase inhibitors** that increase acetylcholine levels in the brain. - This mechanism is primarily used to improve **cognitive function** in patients with **Alzheimer's disease** and other forms of dementia. *Dissociation* - Dissociation involves a mental process causing a lack of connection between thoughts, memory, and identity, and is not typically treated with cholinesterase inhibitors. - Management often involves **psychotherapy** and sometimes anti-anxiety medications or antidepressants, if comorbid conditions are present. *Delusions* - Delusions are fixed, false beliefs often associated with psychotic disorders like **schizophrenia** or severe mood disorders. - Treatment primarily involves **antipsychotic medications**, not acetylcholinesterase inhibitors. *Depression* - Depression is a mood disorder characterized by persistent sadness and loss of interest. - It is typically treated with **antidepressants** (e.g., SSRIs, SNRIs), psychotherapy, or lifestyle changes, none of which include rivastigmine or donepezil.

Question 10: A diabetic female on Isoniazid (INH) and Rifampicin for tuberculosis developed Deep Vein Thrombosis (DVT). She was started on Warfarin, but her Prothrombin Time (PT) is not elevated. What is the next appropriate step in management?

A. Increase the dose of Warfarin
B. Replace Warfarin with Acenocoumarol
C. Switch Ethambutol for Rifampicin
D. Use Low Molecular Weight Heparin (LMWH) (Correct Answer)

Explanation: ### Explanation **1. Why LMWH is the Correct Choice:** The patient is taking **Rifampicin**, a potent **cytochrome P450 (CYP3A4 and CYP2C9) enzyme inducer**. Warfarin is metabolized by these enzymes; therefore, Rifampicin significantly increases Warfarin metabolism, leading to subtherapeutic levels and a failure to elevate the Prothrombin Time (PT/INR). In the acute management of DVT, achieving rapid and reliable anticoagulation is critical [1]. Since the drug interaction makes Warfarin unpredictable and difficult to titrate, switching to **Low Molecular Weight Heparin (LMWH)** is the most appropriate step. LMWH does not rely on the CYP450 system and provides immediate, predictable anticoagulation [2]. **2. Analysis of Incorrect Options:** * **Option A (Increase Warfarin dose):** While theoretically possible, the induction effect of Rifampicin is so profound that extremely high doses of Warfarin would be required, making the INR highly unstable and increasing the risk of toxicity if Rifampicin is later discontinued. * **Option B (Replace with Acenocoumarol):** Acenocoumarol is also a Vitamin K antagonist metabolized by the liver; it shares the same metabolic pathways and drug interactions as Warfarin [1]. * **Option C (Switch Ethambutol for Rifampicin):** Rifampicin is a cornerstone of Short Course Chemotherapy (SCC) for TB. It should not be discontinued or replaced with a less potent drug like Ethambutol solely to accommodate Warfarin, as this risks treatment failure or MDR-TB. **3. NEET-PG High-Yield Pearls:** * **Rifampicin:** The "Great Inducer." It reduces the efficacy of Warfarin, Oral Contraceptive Pills (OCPs), Sulfonylureas, and Digoxin. * **Isoniazid (INH):** Conversely, INH is a CYP enzyme **inhibitor**, but in this clinical scenario, the inducing effect of Rifampicin dominates. * **Management Rule:** When a patient on Rifampicin requires anticoagulation, LMWH or Fondaparinux are preferred over Vitamin K antagonists due to predictable pharmacokinetics [2].

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