Clinical Pharmacology and Drug Toxicity Practice Questions

Q: Acetylsalicylate poisoning causes:

Metabolic acidosis with respiratory alkalosis. ***Metabolic acidosis with respiratory alkalosis due to aspirin toxicity*** - Acetylsalicylate (aspirin) poisoning typically leads to a **mixed acid-base disorder** consisting of primary **metabolic acidosis** and primary **respiratory alkalosis**. - The metabolic acidosis is due to aspirin's direct acid effects and interference with metabolism, while respiratory alkalosis results from aspirin's direct stimulation of the **respiratory center in the medulla**, causing hyperventilation. *Metabolic acidosis due to lactic acidosis, without respiratory compensation.* - While **metabolic acidosis** (often with a component of **lactic acidosis**) is a feature of aspirin toxicity, this option mistakenly suggests the absence of **respiratory compensation**. - **Respiratory alkalosis** is a prominent and often initial feature of aspirin poisoning due to hyperventilation. *Respiratory acidosis with metabolic alkalosis.* - This is an **incorrect combination** for aspirin poisoning. Aspirin generally causes **hyperventilation**, leading to **respiratory alkalosis**, not acidosis. - **Metabolic alkalosis** is also not a direct consequence of aspirin overdose. *Respiratory alkalosis alone.* - While **respiratory alkalosis** is an **initial and key feature** of aspirin poisoning, it is rarely the *only* acid-base disturbance. - The acid effects of salicylates and their metabolic products quickly lead to a concurrent **metabolic acidosis**, making a mixed disorder more common.

Q: What is the treatment of choice for Lalita, a 26-year-old female who accidentally took 100 tablets of paracetamol?

Acetyl cysteine. ***Acetyl cysteine*** - **Acetyl cysteine** is the **antidote** of choice for paracetamol (acetaminophen) overdose. - It works by replenishing **glutathione stores**, which are essential for detoxifying the toxic metabolite of paracetamol, **N-acetyl-p-benzoquinone imine (NAPQI)**. *Gastric lavage* - **Gastric lavage** is generally not recommended for paracetamol overdose unless performed within **1 hour** of ingestion, and even then, its effectiveness is limited. - It carries risks such as aspiration and esophageal injury, making it less favorable than activated charcoal. *Hemodialysis* - **Hemodialysis** is generally reserved for severe cases of paracetamol overdose with life-threatening complications like **severe metabolic acidosis** or **renal failure**, and when acetyl cysteine treatment is delayed or ineffective. - Paracetamol itself is dialyzable, but hemodialysis is not the primary treatment for uncomplicated overdose. *Alkaline diuresis* - **Alkaline diuresis** is a treatment used for overdoses of **weak acids**, such as salicylates or phenobarbital, to enhance their renal excretion. - Paracetamol is not a weak acid, so alkaline diuresis would not be effective in eliminating it from the body.

Q: Which drug is least likely to cause exanthematous skin eruptions?

Hydrocortisone. ***Hydrocortisone*** - **Corticosteroids** like hydrocortisone are **anti-inflammatory** and immunosuppressive agents. - They are commonly used to **treat allergic reactions** and skin eruptions, making them highly unlikely to cause exanthematous eruptions themselves. *Phenytoin* - **Anticonvulsant** medications like phenytoin are frequently associated with various **drug-induced skin reactions**, including exanthematous eruptions. - It is a common cause of **drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome**, which manifests with a widespread rash. *Ampicillin* - **Antibiotics**, particularly **aminopenicillins** like ampicillin, are well-known triggers for **maculopapular rashes** and other exanthematous eruptions. - The incidence of ampicillin-induced rash is notably higher, especially in patients with **viral infections** like infectious mononucleosis. *Phenylbutazone* - This **non-steroidal anti-inflammatory drug (NSAID)** has a documented history of causing severe cutaneous adverse reactions, including **exanthematous eruptions**. - Due to its potential for serious side effects, such as **aplastic anemia** and severe skin reactions, its use is now highly restricted.

Q: What is the drug of choice for treating lithium-induced nephrogenic diabetes insipidus?

Amiloride. ***Amiloride*** - **Amiloride** is the **drug of choice** for lithium-induced nephrogenic diabetes insipidus (Li-NDI). - It blocks the **epithelial sodium channels (ENaC)** in the collecting duct principal cells, thereby **reducing lithium entry** into these cells and decreasing its nephrotoxic effects. - Crucially, amiloride does **NOT increase serum lithium levels**, making it safer than thiazides for long-term management. - It effectively reduces **polyuria and polydipsia** while allowing continued lithium therapy for psychiatric conditions. *Thiazide diuretics* - **Thiazide diuretics** can reduce urine output by causing volume depletion, which increases proximal tubular reabsorption of both water and sodium. - However, this also leads to **increased reabsorption of lithium**, resulting in **elevated serum lithium levels** and potential **lithium toxicity**. - They are considered **second-line therapy** or used in combination with amiloride when monotherapy is insufficient. - The risk of lithium toxicity limits their use as first-line treatment. *Demeclocycline* - **Demeclocycline** is a tetracycline antibiotic that **induces** nephrogenic diabetes insipidus by antagonizing ADH action at renal tubules. - It is used to treat **SIADH** (syndrome of inappropriate antidiuretic hormone secretion), not nephrogenic diabetes insipidus. - Using it would worsen the condition, not treat it. *Indomethacin* - **Indomethacin** is an NSAID that inhibits prostaglandin synthesis, which can reduce urine output in some cases of nephrogenic diabetes insipidus. - It is considered a **third-line option** due to significant side effects including **renal dysfunction**, **gastric ulceration**, and **cardiovascular risks**. - Reserved for cases where amiloride and thiazides have failed or are contraindicated.

Q: Which of the following is not a recommended treatment for lithium toxicity?

Acidification of urine. ***Acidification of urine*** - **Lithium** is primarily excreted by the kidneys unchanged, and its renal handling is influenced by sodium and water balance, not urinary pH changes. - Urinary acidification is effective for enhancing elimination of **weak bases** (e.g., amphetamines), but lithium is **not ionizable** and its excretion is pH-independent. - This intervention is **ineffective for lithium toxicity** and could potentially worsen electrolyte imbalances. *Increased hydration* - **Increased hydration** with intravenous normal saline is a cornerstone of lithium toxicity management. - Saline infusion helps to **restore intravascular volume**, improve GFR, and reduce proximal tubular reabsorption of lithium (lithium is reabsorbed along with sodium) [1]. - This intervention effectively **lowers serum lithium levels** in mild-to-moderate toxicity. *Sodium bicarbonate* - **Sodium bicarbonate** is NOT a standard treatment for lithium toxicity. - Unlike drugs eliminated by ion trapping (salicylates, methotrexate), lithium excretion is **not enhanced by urinary alkalinization**. - While sodium administration (via saline) helps lithium excretion, the bicarbonate component provides no additional benefit over normal saline and may cause metabolic alkalosis. - Sodium bicarbonate may be used if metabolic **acidosis** is present as a complication, but not as a primary treatment for lithium toxicity itself. *Hemodialysis* - **Hemodialysis** is the most effective and definitive treatment for severe lithium toxicity (serum levels >4 mEq/L, severe symptoms, renal failure, or deteriorating clinical status). - Lithium has ideal characteristics for dialysis: **low molecular weight** (7 Da), minimal protein binding (<10%), and small volume of distribution (0.7-0.9 L/kg). - Can rapidly reduce serum lithium levels by **50% or more** per session.

Q: Which of the following is the most commonly reported pharmacological agent causing peliosis hepatis?

Anabolic steroids. ***Anabolic steroids*** - **Anabolic androgenic steroids** are consistently linked to peliosis hepatis, a condition characterized by **blood-filled cysts** within the liver. - The liver damage resulting from anabolic steroid use is often **dose-dependent** and can also lead to other complications like **hepatic adenomas** and **cholestasis**. *Methotrexate* - While methotrexate is a known cause of **hepatotoxicity**, it typically manifests as **fibrosis** and **cirrhosis**, not peliosis hepatis. - Its mechanism of liver injury involves direct cellular damage, distinct from the **vascular changes** seen in peliosis hepatis. *Pyrazinamide* - Pyrazinamide is an **anti-tuberculosis drug** well-known for its potential to cause **hepatocellular injury**, leading to **elevated liver enzymes** and **hepatitis**. - Its primary liver pathology does not involve the formation of **blood-filled cysts** characteristic of peliosis hepatis. *Interferon Alpha* - Interferon alpha can cause various adverse effects, including **flu-like symptoms**, **myelosuppression**, and **neuropsychiatric effects**. - While it can impact liver function, severe **hepatic vascular disorders** like peliosis hepatis are **not commonly associated** with its use.

Q: Sterile pyuria may occur due to:

Phenytoin. ***Phenytoin*** - **Phenytoin** is a well-known cause of **drug-induced acute interstitial nephritis (AIN)**, which is a classic cause of **sterile pyuria**. - **Acute interstitial nephritis** presents with inflammatory infiltration of the renal interstitium, leading to pyuria (white blood cells in urine) **without bacterial infection**. - Other features of drug-induced AIN include fever, rash, eosinophilia, and acute kidney injury. - Phenytoin, along with other drugs like penicillins, NSAIDs, and rifampicin, can trigger this hypersensitivity-mediated renal injury. *Paracetamol* - **Paracetamol (acetaminophen)** overdose causes **acute tubular necrosis (ATN)**, not interstitial nephritis. - ATN primarily presents with acute kidney injury, oliguria, and elevated creatinine, but **sterile pyuria is not a characteristic feature** of ATN. - The renal damage is direct tubular cell injury rather than inflammatory interstitial infiltration. *Lignocaine* - **Lignocaine (lidocaine)** is a local anesthetic and antiarrhythmic agent with side effects primarily affecting the **central nervous system and cardiovascular system**. - It is **not associated with renal toxicity** or sterile pyuria. *Cocaine* - **Cocaine** can cause kidney damage through **rhabdomyolysis**, **vasoconstriction**, and **hypertensive crisis**, leading to **acute kidney injury**. - While cocaine-related AKI can occur, it does not typically cause **drug-induced interstitial nephritis** or classic sterile pyuria. - Renal injury from cocaine is usually related to ischemic or myoglobinuric mechanisms rather than inflammatory infiltration.

Q: Which one of the following nonsteroidal anti-inflammatory drugs has adverse effects on the liver?

Diclofenac Sodium. ***Diclofenac Sodium*** - **Diclofenac** is the NSAID most commonly associated with **hepatotoxicity** among commonly prescribed NSAIDs - Can cause **elevated liver enzymes** (transaminases) and in rare cases **severe hepatotoxicity** leading to acute liver failure - Has **black box warnings** in many countries regarding hepatic adverse effects - **Regular monitoring of liver function tests** is recommended for patients on long-term diclofenac therapy - Hepatotoxicity risk is dose-dependent and more common with prolonged use *Aspirin* - Aspirin (acetylsalicylic acid) is an NSAID with primary adverse effects related to **gastrointestinal irritation**, **bleeding**, and **antiplatelet effects** - In children, associated with **Reye's syndrome** (hepatic encephalopathy) - Very high doses or chronic use can cause mild, reversible liver enzyme elevations, but **significant hepatotoxicity is uncommon** in adults - Not prominently associated with liver toxicity compared to diclofenac *Ibuprofen* - Ibuprofen is a well-tolerated NSAID with most common adverse effects being **gastrointestinal discomfort**, **peptic ulcers**, and **renal impairment** - Although NSAIDs as a class can rarely cause idiosyncratic liver injury, ibuprofen has a **very low incidence of hepatotoxicity** - Considered one of the safer NSAIDs regarding hepatic effects *Naproxen* - Naproxen is a commonly used NSAID with primary adverse effects similar to other NSAIDs: **gastrointestinal irritation** and **renal effects** - Hepatotoxicity is **rare** with naproxen compared to diclofenac - Generally well-tolerated with respect to liver function - Idiosyncratic liver injury can occur but is uncommon

Q: Methemoglobinemia is associated with:

Prilocaine. ***Prilocaine*** - **Prilocaine** is a local anesthetic known to cause **methemoglobinemia** at higher doses due to its metabolite, **o-toluidine**. - This metabolite oxidizes iron in hemoglobin from the ferrous (Fe2+) to the ferric (Fe3+) state, rendering it unable to bind oxygen. *Aminoester local anesthetic* - While some aminoester local anesthetics can cause allergic reactions, they are not typically associated with **methemoglobinemia**. - **Methemoglobinemia** is more commonly linked with aminoamide local anesthetics containing specific chemical structures. *Bupivacaine* - **Bupivacaine** is an aminoamide local anesthetic primarily known for its potential to cause **cardiotoxicity** at high systemic concentrations. - It does not commonly induce **methemoglobinemia**. *Mepivacaine* - **Mepivacaine** is another aminoamide local anesthetic, chemically similar to lidocaine. - While it can cause CNS toxicity and cardiovascular effects at high doses, it is not a significant cause of **methemoglobinemia**.

Question 1

Acetylsalicylate poisoning causes:

Accepted Answer

Metabolic acidosis with respiratory alkalosis

Answer

Respiratory acidosis with metabolic alkalosis.

Answer

Respiratory alkalosis alone.

Answer

Metabolic acidosis due to lactic acidosis, without respiratory compensation.

Question 2

What is the treatment of choice for Lalita, a 26-year-old female who accidentally took 100 tablets of paracetamol?

Accepted Answer

Acetyl cysteine

Answer

Gastric lavage

Answer

Hemodialysis

Answer

Alkaline diuresis

Question 3

Which drug is least likely to cause exanthematous skin eruptions?

Accepted Answer

Hydrocortisone

Answer

Phenytoin

Answer

Ampicillin

Answer

Phenylbutazone

Question 4

What is the drug of choice for treating lithium-induced nephrogenic diabetes insipidus?

Accepted Answer

Amiloride

Answer

Demeclocycline

Answer

Indomethacin

Answer

Thiazide diuretics

Question 5

Which of the following is not a recommended treatment for lithium toxicity?

Accepted Answer

Acidification of urine

Answer

Increased hydration

Answer

Hemodialysis

Answer

Sodium bicarbonate

Question 6

Which of the following is the most commonly reported pharmacological agent causing peliosis hepatis?

Accepted Answer

Anabolic steroids

Answer

Methotrexate

Answer

Pyrazinamide

Answer

Interferon Alpha

Question 7

A woman consumes several tablets of amitriptyline (a case of amitriptyline poisoning). Which of the following is NOT an appropriate management step?

Accepted Answer

Atropine as antidote

Answer

Gastric lavage

Answer

Sodium bicarbonate infusion

Answer

Activated charcoal administration

Question 8

Sterile pyuria may occur due to:

Accepted Answer

Phenytoin

Answer

Cocaine

Answer

Lignocaine

Answer

Paracetamol

Question 9

Which one of the following nonsteroidal anti-inflammatory drugs has adverse effects on the liver?

Accepted Answer

Diclofenac Sodium

Answer

Aspirin

Answer

Ibuprofen

Answer

Naproxen

Question 10

Methemoglobinemia is associated with:

Accepted Answer

Prilocaine

Answer

Aminoester local anesthetic

Answer

Bupivacaine

Answer

Mepivacaine

Clinical Pharmacology and Drug Toxicity — MCQs

Clinical Pharmacology and Drug Toxicity — MCQs

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