Clinical Pharmacology and Drug Toxicity — MCQs
On this page
A 60-year-old female presented with left jaw pain and fever. Examination revealed poor dentition, a purulent drainage area in the mouth, right-sided facial swelling, and diffuse mandibular tenderness. Her medication history includes alendronate and lisinopril. Microscopic examination of purulent secretions was performed. What is the most appropriate drug for this condition?
Hyperkalemia is not caused by which of the following medications?
All of the following cause hyperglycemia, EXCEPT?
Which of the following drugs does not cause renal toxicity?
BAL is used as an antidote for poisoning by which of the following substances?
Which is the only local anesthetic that raises blood pressure?
Which of the following does not cause hemolysis in G6PD deficiency?
Patisiran was approved by FDA recently for which condition?
What is the immediate emergency treatment for CO poisoning?
Fomepizole is used as an antidote in poisoning by which of the following substances?
Clinical Pharmacology and Drug Toxicity Indian Medical PG Practice Questions and MCQs
Question 31: A 60-year-old female presented with left jaw pain and fever. Examination revealed poor dentition, a purulent drainage area in the mouth, right-sided facial swelling, and diffuse mandibular tenderness. Her medication history includes alendronate and lisinopril. Microscopic examination of purulent secretions was performed. What is the most appropriate drug for this condition?
- A. Penicillin (Correct Answer)
- B. Azithromycin
- C. Griseofulvin
- D. Metronidazole
Explanation: ### Explanation **Diagnosis: Actinomycosis (Lumpy Jaw)** The clinical presentation of a subacute/chronic infection involving the jaw, characterized by **purulent drainage**, facial swelling, and mandibular tenderness in a patient with poor dentition, is classic for **Actinomycosis**. While the patient is on alendronate (raising suspicion for Bisphosphonate-Related Osteonecrosis of the Jaw), the presence of fever and purulent secretions strongly points toward an infectious etiology, specifically *Actinomyces israelii*. **Why Penicillin is Correct:** *Actinomyces* species are Gram-positive, anaerobic, filamentous bacteria (not fungi). **High-dose Penicillin G** (intravenous followed by oral Penicillin V) is the **drug of choice** for Actinomycosis. Treatment is typically prolonged (6–12 months) to prevent recurrence due to the bacteria's tendency to form dense colonies and cross tissue planes. **Why Other Options are Incorrect:** * **B. Azithromycin:** While macrolides can be used in penicillin-allergic patients, they are not the first-line treatment. * **C. Griseofulvin:** This is an antifungal agent used for dermatophytosis (tinea). *Actinomyces* is a bacterium, despite its "fungus-like" branching appearance. * **D. Metronidazole:** Although *Actinomyces* is an anaerobe, it is uniquely **resistant to metronidazole**. This is a high-yield distinction from other anaerobic infections. **NEET-PG High-Yield Pearls:** 1. **Sulfur Granules:** Microscopic examination of the pus often reveals yellow "sulfur granules," which are actually masses of filamentous organisms. 2. **Molar Tooth Sign:** On culture (Agar), *Actinomyces* colonies often resemble the shape of a molar tooth. 3. **Tissue Planes:** Actinomycosis is known for ignoring anatomical boundaries, leading to sinus tract formation. 4. **Differential:** Always differentiate from **BRONJ** (Bisphosphonate-Related Osteonecrosis of the Jaw) in patients on alendronate; however, the presence of "sulfur granules" or purulence confirms Actinomycosis.
Question 32: Hyperkalemia is not caused by which of the following medications?
- A. Salbutamol (Correct Answer)
- B. ACE Inhibitors
- C. Cyclosporine
- D. GM-CSF
Explanation: ### Explanation The correct answer is **Salbutamol**. **1. Why Salbutamol is the correct answer:** Salbutamol is a **$\beta_2$-adrenergic agonist**. Stimulation of $\beta_2$ receptors activates the Na⁺/K⁺-ATPase pump, which shifts potassium from the extracellular fluid into the intracellular compartment (primarily into skeletal muscle). This results in **hypokalemia**, not hyperkalemia. Due to this mechanism, nebulized salbutamol is clinically used as an emergency treatment to lower serum potassium levels in patients with hyperkalemia. **2. Why the other options are incorrect:** * **ACE Inhibitors (e.g., Enalapril):** These drugs inhibit the synthesis of Angiotensin II, leading to decreased secretion of **Aldosterone**. Since aldosterone is responsible for potassium excretion in the distal tubule, its deficiency leads to potassium retention (**Hyperkalemia**). * **Cyclosporine:** This calcineurin inhibitor causes **Hyperkalemia** by suppressing aldosterone synthesis and inducing tubular resistance to aldosterone. It also interferes with the ROMK (Renal Outer Medullary Potassium) channels. * **GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor):** A less common but high-yield fact is that GM-CSF can cause **Hyperkalemia** as a side effect, often associated with rapid cell turnover or lysis (Tumor Lysis Syndrome-like effect) or renal effects. **3. NEET-PG High-Yield Pearls:** * **Drugs causing Hyperkalemia (K-BANK):** **K**-sparing diuretics (Spironolactone), **B**eta-blockers (non-selective), **A**CE inhibitors/ARBs, **N**SAIDs, and **K**-supplementation/Heparin/Cyclosporine. * **Drugs causing Hypokalemia:** $\beta_2$ agonists, Insulin, Diuretics (Thiazides/Loop), and Amphotericin B. * **Management of Hyperkalemia:** "C BIG K" — **C**alcium gluconate (cardioprotection), **B**icarbonate/ **B**eta-agonists, **I**nsulin + **G**lucose, **K**ayexalate (Resins), and Dialysis.
Question 33: All of the following cause hyperglycemia, EXCEPT?
- A. Thiazide
- B. Diazoxide
- C. Theophylline (Correct Answer)
- D. Pentamidine
Explanation: Explanation: The correct answer is Theophylline. In cases of acute toxicity, Theophylline typically causes hypokalemia and hyperglycemia (due to catecholamine release). However, it is not classically categorized as a drug that induces clinical hyperglycemia or diabetes mellitus as a side effect. In fact, among the options provided, it is the least likely to be associated with persistent elevated blood glucose levels. Analysis of Options: * Thiazide Diuretics (A): These are notorious for causing hyperglycemia. They inhibit insulin release from the pancreas (via K+ channel activation) [1] and decrease peripheral glucose utilization, often worsening glycemic control in diabetics. * Diazoxide (B): This drug is a potent K+ATP channel opener in pancreatic beta cells. [2] By keeping these channels open, it hyperpolarizes the cell and inhibits insulin secretion. [2] It is clinically used to treat hypoglycemia in conditions like insulinoma. * Pentamidine (D): This is a high-yield "double-edged sword" for NEET-PG. It is initially cytotoxic to pancreatic beta cells. This causes an initial massive release of insulin (leading to hypoglycemia), followed by permanent beta-cell destruction, resulting in insulin-dependent diabetes mellitus (hyperglycemia). Clinical Pearls for NEET-PG: * Drugs causing Hyperglycemia: Steroids, Thiazides, Diazoxide, Protease Inhibitors, Phenytoin, Beta-blockers, and Niacin. * Pentamidine Paradox: Remember the sequence: Acute Hypoglycemia → Chronic Hyperglycemia. * Theophylline Toxicity: Focus on the triad of Seizures, Arrhythmias, and Hypokalemia. While hyperglycemia can occur in acute overdose, it is not a standard metabolic side effect of the drug.
Question 34: Which of the following drugs does not cause renal toxicity?
- A. Cisplatin
- B. Cisplatin
- C. Mycophenolate mofetil (Correct Answer)
- D. Methotrexate
Explanation: **Explanation:** The correct answer is **Mycophenolate mofetil (MMF)**. **Why Mycophenolate mofetil is correct:** MMF is an immunosuppressant that acts by inhibiting **inosine monophosphate dehydrogenase (IMPDH)**, the rate-limiting enzyme in the *de novo* synthesis of guanosine nucleotides. Since T and B lymphocytes are uniquely dependent on this pathway (unlike other cells that use the salvage pathway), MMF is highly selective for lymphocytes. Its primary toxicities are **gastrointestinal (diarrhea, vomiting)** and **hematological (leukopenia)**. Crucially, it lacks nephrotoxicity, making it a preferred agent in renal transplant patients to avoid the renal damage associated with Calcineurin inhibitors (like Cyclosporine). **Why the other options are incorrect:** * **Cisplatin:** This is a platinum-based antineoplastic agent notorious for causing **dose-limiting nephrotoxicity** (specifically acute tubular necrosis). It accumulates in the proximal convoluted tubules. Amifostine is often used as a cytoprotective agent to reduce this risk. * **Methotrexate:** High doses of this folate antagonist can cause renal toxicity due to the **precipitation of the drug and its metabolites (7-OH-methotrexate)** in the renal tubules, leading to crystalluria and obstructive uropathy. Vigorous hydration and urinary alkalinization are required during therapy. **NEET-PG High-Yield Pearls:** * **Drug of choice for preventing nephrotoxicity:** *Amifostine* for Cisplatin; *Mesna* for Cyclophosphamide (hemorrhagic cystitis). * **Common Nephrotoxic Drugs:** Aminoglycosides, Amphotericin B, NSAIDs, Contrast media, and Calcineurin inhibitors (Tacrolimus/Cyclosporine). * **MMF Advantage:** Unlike Cyclosporine, MMF does not cause hypertension, hirsutism, or gingival hyperplasia.
Question 35: BAL is used as an antidote for poisoning by which of the following substances?
- A. Morphine
- B. Aconite
- C. Phenol
- D. Mercury (Correct Answer)
Explanation: **Explanation:** **BAL (British Anti-Lewisite)**, also known as **Dimercaprol**, is a chelating agent containing two sulfhydryl (-SH) groups. It is the correct answer because it is specifically designed to treat heavy metal poisoning, including **Mercury**, Arsenic, and Gold. 1. **Mechanism of Action:** Heavy metals exert their toxicity by binding to and inactivating essential sulfhydryl-containing enzymes in the body. BAL acts as a "decoy" by providing competing sulfhydryl groups. The metal binds to BAL to form a stable, non-toxic, water-soluble heterocyclic ring complex that is subsequently excreted in the urine. 2. **Why other options are incorrect:** * **Morphine:** This is an opioid. The specific antidote is **Naloxone** (a pure opioid antagonist). * **Aconite:** This is a cardiac and nerve poison. There is no specific antidote; treatment is primarily symptomatic (atropine for bradycardia, anti-arrhythmics). * **Phenol:** This is a corrosive. Treatment involves immediate washing of the skin with PEG (Polyethylene glycol) or water and supportive care; chelating agents like BAL have no role here. **High-Yield Clinical Pearls for NEET-PG:** * **Administration:** BAL must be administered via **deep intramuscular (IM)** injection because it is dispensed in peanut oil. * **Contraindications:** It is contraindicated in patients with **G6PD deficiency** (causes hemolysis) and **peanut allergies**. * **Iron Poisoning:** BAL should **not** be used for Iron poisoning as the BAL-Iron complex is itself nephrotoxic. * **Lead Poisoning:** In severe lead encephalopathy, BAL is used in combination with Edetate calcium disodium (CaNa₂EDTA).
Question 36: Which is the only local anesthetic that raises blood pressure?
- A. Lignocaine
- B. Cocaine (Correct Answer)
- C. Prilocaine
- D. Lidocaine
Explanation: **Explanation:** **Cocaine** is unique among local anesthetics because it is the only one that acts as a **vasoconstrictor** and causes an increase in blood pressure. **Mechanism of Action:** Most local anesthetics are vasodilators. However, cocaine inhibits the reuptake of catecholamines (norepinephrine, epinephrine, and dopamine) at the pre-synaptic nerve terminals (NET/uptake-1). This leads to an accumulation of norepinephrine in the synaptic cleft, resulting in potent stimulation of alpha and beta-adrenergic receptors. The alpha-1 stimulation causes peripheral vasoconstriction, leading to hypertension and localized ischemia, while beta-1 stimulation causes tachycardia. **Analysis of Incorrect Options:** * **Lignocaine (Lidocaine):** These are the same drug (Option A and D). Lidocaine is an amide-linked local anesthetic that causes peripheral vasodilation by relaxing vascular smooth muscle. It is often co-administered with adrenaline to counteract this effect. * **Prilocaine:** Like most other amides, it causes vasodilation. It is clinically significant for causing **methemoglobinemia** due to its metabolite, o-toluidine, but it does not raise blood pressure. **High-Yield NEET-PG Pearls:** * **Cocaine Toxicity:** Can lead to coronary vasospasm, myocardial infarction, and cardiac arrhythmias. * **Contraindication:** Never use **Beta-blockers** alone in cocaine toxicity; "unopposed alpha stimulation" can lead to a hypertensive crisis. * **Ester vs. Amide:** Cocaine is an ester-linked local anesthetic. * **Surface Anesthesia:** Due to its intrinsic vasoconstrictive properties, cocaine is the only local anesthetic that does not require the addition of adrenaline for topical use (e.g., in ENT procedures).
Question 37: Which of the following does not cause hemolysis in G6PD deficiency?
- A. Estrogen (Correct Answer)
- B. Salicylates
- C. Primaquine
- D. Nitrofurantoin
Explanation: ### Explanation **Concept Overview:** Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is an X-linked recessive disorder where RBCs lack the enzyme necessary to maintain levels of reduced glutathione. Reduced glutathione is essential for neutralizing reactive oxygen species (ROS). When patients are exposed to oxidative stress (drugs, infections, or fava beans), hemoglobin denatures into **Heinz bodies**, leading to hemolysis. **Why Estrogen is the Correct Answer:** * **Estrogen (Option A):** Estrogen and other hormonal preparations (like oral contraceptives) do not possess oxidative properties and do not interfere with the pentose phosphate pathway. Therefore, they do not trigger hemolytic episodes in G6PD-deficient individuals. **Why the Other Options are Incorrect:** * **Primaquine (Option C):** This is the classic "prototype" drug that causes hemolysis. It is an antimalarial that generates significant oxidative stress. Testing for G6PD deficiency is mandatory before prescribing Primaquine. * **Nitrofurantoin (Option D):** A common urinary antiseptic that undergoes redox cycling, producing superoxide radicals that overwhelm the limited antioxidant capacity of G6PD-deficient cells. * **Salicylates (Option B):** High doses of aspirin or salicylates can induce oxidative damage to RBC membranes, though they are considered "low-risk" compared to Primaquine, they are still documented triggers. **NEET-PG High-Yield Pearls:** * **Mnemonic for G6PD Triggers:** "**S**ell **P**ie **N**ow" (**S**ulfonamides/Salicylates, **P**rimaquine, **N**itrofurantoin). * **Peripheral Smear Findings:** Look for **Heinz Bodies** (denatured Hb) and **Bite Cells** (deformed RBCs after splenic macrophages remove Heinz bodies). * **Other Triggers:** Dapsone, Chloroquine, Rasburicase, and Fava beans (Favism). * **Inheritance:** X-linked recessive; more common in males of Mediterranean or African descent.
Question 38: Patisiran was approved by FDA recently for which condition?
- A. Filariasis
- B. Peripheral Neuropathy
- C. Neuropathy of diabetes
- D. Neuropathy of amyloidosis (Correct Answer)
Explanation: **Explanation:** **Patisiran** is a groundbreaking medication that represents the first-ever FDA-approved drug (2018) utilizing **RNA interference (RNAi)** technology [2]. **Why Option D is correct:** Patisiran is specifically indicated for the treatment of polyneuropathy caused by **Hereditary Transthyretin-mediated (hATTR) Amyloidosis**. In this condition, mutations in the TTR gene lead to the accumulation of misfolded amyloid proteins in peripheral nerves. Patisiran consists of a **small interfering RNA (siRNA)** formulated in lipid nanoparticles [2]. It works by binding to and degrading the messenger RNA (mRNA) responsible for producing the transthyretin (TTR) protein in the liver, thereby reducing amyloid deposits in tissues and improving neurological symptoms. **Why other options are incorrect:** * **A. Filariasis:** This is a parasitic infection treated with anthelmintics like Diethylcarbamazine (DEC) or Ivermectin. * **B. Peripheral Neuropathy:** This is a broad clinical symptom, not a specific disease entity. Patisiran is only indicated for the specific amyloid-related subtype. [3] * **C. Neuropathy of diabetes:** The most common cause of neuropathy, usually managed with glycemic control and symptomatic drugs like Pregabalin, Duloxetine, or Amitriptyline. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** RNA interference (gene silencing) [2]. * **Route:** Intravenous infusion. * **Related Drug:** **Inotersen** is another drug for hATTR, but it is an *antisense oligonucleotide* (ASO), not an siRNA [2]. * **Side Effects:** Infusion-related reactions and Vitamin A deficiency (as TTR normally transports Vitamin A; supplementation is required).
Question 39: What is the immediate emergency treatment for CO poisoning?
- A. 5% CO2 inhalation
- B. 10% CO2 inhalation
- C. High flow O2 (Correct Answer)
- D. Nitroglycerine
Explanation: **Explanation:** **1. Why High Flow O2 is Correct:** Carbon Monoxide (CO) has an affinity for hemoglobin that is **200–250 times higher** than that of oxygen. When CO binds to hemoglobin, it forms **Carboxyhemoglobin (COHb)**, which shifts the oxygen-dissociation curve to the **left**, preventing the release of oxygen to tissues (cellular hypoxia) [1]. The primary goal of treatment is to displace CO from hemoglobin. The half-life of COHb is approximately 4–6 hours on room air. Administering **100% High Flow Oxygen** (via a non-rebreather mask) reduces this half-life to about **60–90 minutes**. In severe cases (e.g., COHb >25%, pregnancy, or neurological symptoms), **Hyperbaric Oxygen (HBO)** is used, further reducing the half-life to ~20 minutes. **2. Why Other Options are Incorrect:** * **Options A & B (CO2 Inhalation):** Historically, Carbogen (95% O2 + 5% CO2) was suggested to stimulate the respiratory center. However, CO2 can worsen respiratory acidosis and is no longer recommended in emergency protocols [2]. * **Option D (Nitroglycerine):** This is a vasodilator used in angina/MI. It has no role in CO poisoning and may worsen hypotension in a critically ill patient. **3. High-Yield Clinical Pearls for NEET-PG:** * **Classic Presentation:** "Cherry-red" skin/mucosa (rare in life, common post-mortem), headache, and confusion. * **Diagnosis:** Pulse oximetry is **unreliable** (it cannot distinguish between oxyhemoglobin and carboxyhemoglobin) [3]. Diagnosis is confirmed via **ABG/VBG with Co-oximetry**. * **CT/MRI Finding:** Bilateral necrosis of the **Globus Pallidus** is a characteristic late finding. * **Mechanism:** CO also binds to **Cytochrome a3**, inhibiting the mitochondrial electron transport chain.
Question 40: Fomepizole is used as an antidote in poisoning by which of the following substances?
- A. Organophosphorus compounds
- B. Methanol (Correct Answer)
- C. Aluminium phosphide
- D. Copper
Explanation: **Explanation:** **Correct Answer: B. Methanol** Fomepizole is a potent competitive inhibitor of the enzyme **Alcohol Dehydrogenase (ADH)** [1]. In methanol poisoning, the toxicity is not caused by the methanol itself, but by its metabolite, **formic acid**, which causes metabolic acidosis and retinal damage (blindness) [1]. By inhibiting ADH, Fomepizole prevents the conversion of methanol into formaldehyde and subsequently formic acid, allowing the parent compound to be excreted harmlessly by the kidneys. It is also the antidote of choice for **Ethylene glycol** poisoning [1]. **Incorrect Options:** * **A. Organophosphorus compounds:** These are treated with **Atropine** (muscarinic antagonist) and **Pralidoxime/PAM** (cholinesterase reactivator) [2]. * **C. Aluminium phosphide:** There is no specific antidote for "Celphos" poisoning. Management is primarily supportive (gastric lavage with KMnO4 and coconut oil, magnesium sulfate). * **D. Copper:** Wilson’s disease or acute copper toxicity is treated with chelating agents like **D-Penicillamine** or Trientine. **High-Yield Clinical Pearls for NEET-PG:** * **Fomepizole vs. Ethanol:** While both inhibit ADH, Fomepizole is preferred over ethanol because it does not cause CNS depression or hypoglycemia and does not require constant blood level monitoring. * **Methanol Triad:** CNS depression, severe metabolic acidosis (high anion gap), and visual disturbances ("snowfield vision") [1]. * **Indication:** Fomepizole is indicated when the plasma methanol concentration is >20 mg/dL or if there is a documented osmolar gap with metabolic acidosis.
Practice by Chapter
Principles of Clinical Pharmacology
Practice Questions
Therapeutic Drug Monitoring
Practice Questions
Drug Toxicity and Overdose
Practice Questions
Antidotes and Their Applications
Practice Questions
Management of Drug Poisoning
Practice Questions
Drug-Induced Liver Injury
Practice Questions
Drug-Induced Kidney Injury
Practice Questions
Drug-Induced Blood Dyscrasias
Practice Questions
Drug-Induced QT Prolongation
Practice Questions
Pharmacovigilance
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free