Botulinum toxin type B is used in which disease?
Which one of the following agents has been associated with hemorrhagic stroke?
Which of the following drugs can cause thyroid dysfunction?
An Englishman travels to a place which is resistant to chloroquine and mefloquine. What should he take as prophylaxis?
Which of the following is a mineralocorticoid antagonist?
Thiazides act on which part of the nephron?
What are the primary mechanisms behind cardiac toxicity associated with Tricyclic antidepressants?
Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?
Lithium directly affects which ion ?
Which of the following is a classic tricyclic antidepressant (TCA) commonly used as the prototype for the class?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 81: Botulinum toxin type B is used in which disease?
- A. Cervical dystonia (Correct Answer)
- B. Blepharospasm
- C. Strabismus
- D. Glabellar lines
Explanation: ***Cervical dystonia*** * **Botulinum toxin type B (Myobloc/NeuroBloc)** is specifically approved for the treatment of **cervical dystonia**, which involves involuntary contractions of neck muscles. * It works by blocking the release of **acetylcholine** at the neuromuscular junction, leading to muscle relaxation. *Strabismus* * **Botulinum toxin type A (Botox, Dysport, Xeomin)** is the preferred and most commonly used form for treating **strabismus** by temporarily weakening specific extraocular muscles. * Type B is generally not indicated for strabismus due to differences in potency and duration of action. *Blepharospasm* * **Botulinum toxin type A** (e.g., Botox) is the primary treatment for **blepharospasm**, an involuntary forceful closure of the eyelids. * While both types inhibit acetylcholine release, type A has a more established and concentrated use in treating localized muscle spasms like blepharospasm. *Glabellar lines* * **Botulinum toxin type A** is widely used for cosmetic applications such as reducing **glabellar lines** (frown lines between the eyebrows). * Its efficacy and safety for cosmetic indications are well-established, making type A the standard choice over type B.
Question 82: Which one of the following agents has been associated with hemorrhagic stroke?
- A. Phenylpropanolamine (Correct Answer)
- B. Terfenadine
- C. Quinidine
- D. Fenfluramine
Explanation: ***Phenylpropanolamine*** - **Phenylpropanolamine (PPA)** is a sympathomimetic agent that was formerly used as a nasal decongestant and anorectic. - Its use has been linked to an increased risk of **hemorrhagic stroke**, particularly in young women, due to its **vasoconstrictive effects** and potential to cause a sudden, severe rise in blood pressure. *Terfenadine* - **Terfenadine** is a second-generation antihistamine that was voluntarily withdrawn from the market due to its association with severe **cardiac arrhythmias (QT prolongation and Torsades de Pointes)**, not hemorrhagic stroke. - It works by blocking H1 histamine receptors but also had effects on cardiac potassium channels. *Quinidine* - **Quinidine** is an antiarrhythmic drug (Class Ia) primarily used to treat supraventricular and ventricular arrhythmias. - Its main side effects include **gastrointestinal disturbances**, **cinchonism**, and the risk of **QT prolongation** leading to Torsades de Pointes; it is not typically associated with hemorrhagic stroke. *Fenfluramine* - **Fenfluramine** was an anorectic drug used in the treatment of obesity, often in combination with phentermine. - It was withdrawn from the market due to its association with **pulmonary hypertension** and **cardiac valvulopathy**, not hemorrhagic stroke.
Question 83: Which of the following drugs can cause thyroid dysfunction?
- A. Amiodarone (Correct Answer)
- B. Ampicillin
- C. Ibutilide
- D. Acyclovir
Explanation: ***Amiodarone*** - **Amiodarone** is known to cause both **hypothyroidism** and **hyperthyroidism** due to its high iodine content and direct toxic effects on the thyroid gland. - Its effects can persist for months after discontinuation due to its **long half-life** and accumulation in tissues. *Ampicillin* - **Ampicillin** is an antibiotic that generally does not directly affect thyroid function. - Its primary mechanism of action involves inhibiting **bacterial cell wall synthesis**, with no known significant endocrine side effects. *Ibutilide* - **Ibutilide** is an antiarrhythmic drug used for recent-onset atrial fibrillation or flutter. - It works by blocking potassium channels and has no recognized association with thyroid dysfunction. *Acyclovir* - **Acyclovir** is an antiviral medication used to treat herpes virus infections. - Its mechanism of action involves inhibiting viral DNA replication and it is not known to impact thyroid hormone synthesis or metabolism.
Question 84: An Englishman travels to a place which is resistant to chloroquine and mefloquine. What should he take as prophylaxis?
- A. Primaquine
- B. Atovaquone-proguanil (Correct Answer)
- C. Doxycycline
- D. Proguanil
Explanation: ***Atovaquone-proguanil*** - This combination, known as **Malarone**, is the most appropriate prophylactic agent for areas with **multi-drug resistant malaria**, including resistance to chloroquine and mefloquine [1], [2]. - It targets multiple stages of the parasite life cycle, providing excellent protection and is generally well-tolerated with specific **WHO and CDC recommendations** for chloroquine and mefloquine resistant areas [1], [3]. *Primaquine* - **Primaquine** is primarily used for **causal prophylaxis** against *P. vivax* and *P. ovale* to prevent relapse, not as primary prophylaxis [2]. - It is not typically recommended as the primary prophylactic agent in areas with **chloroquine and mefloquine resistance** and requires **G6PD testing** due to risk of hemolysis [1]. *Proguanil* - While proguanil is used for malaria prophylaxis, **proguanil alone** is not effective enough for prophylaxis in areas with multi-drug resistant malaria. - It is typically used in **combination with atovaquone** rather than as monotherapy for effective protection [3]. *Doxycycline* - **Doxycycline** is also an effective prophylactic agent for areas with **chloroquine and mefloquine-resistant malaria** and is commonly recommended [1], [2]. - While effective, it can cause **photosensitivity** and **gastrointestinal upset**, making atovaquone-proguanil the preferred first-line choice.
Question 85: Which of the following is a mineralocorticoid antagonist?
- A. Spironolactone (Correct Answer)
- B. Inamrinone
- C. Nicorandil
- D. Ketorolac
Explanation: ***Spironolactone*** - **Spironolactone** is a **potassium-sparing diuretic** that acts as a competitive antagonist of **aldosterone** at the mineralocorticoid receptors in the renal tubules [1], [2]. - Its primary use is in conditions like **heart failure**, **cirrhosis with ascites**, and **primary hyperaldosteronism** (Conn's syndrome) [2]. *Inamrinone* - **Inamrinone** is a **phosphodiesterase-3 inhibitor** (PDE3 inhibitor) and is classified as an **inotropic agent**. - It increases **intracellular cAMP** in cardiac cells, leading to increased **contractility** and **vasodilation**, and is used in severe heart failure. *Nicorandil* - **Nicorandil** is a **potassium channel opener** and a **nitrate-like drug** that causes both venous and arterial vasodilation. - It is primarily used as an **antianginal agent** due to its ability to reduce cardiac workload and improve coronary blood flow. *Ketorolac* - **Ketorolac** is a **nonsteroidal anti-inflammatory drug (NSAID)** that primarily inhibits **cyclooxygenase (COX) enzymes**. - It is used for **short-term management of acute moderate to severe pain** and has no direct activity on mineralocorticoid receptors.
Question 86: Thiazides act on which part of the nephron?
- A. Proximal Convoluted Tubule
- B. Descending limb of loop of Henle
- C. Glomerulus
- D. Distal Convoluted Tubule (Correct Answer)
Explanation: ***Distal Convoluted Tubule*** - **Thiazide diuretics** specifically inhibit the **sodium-chloride cotransporter (NCC)** in the apical membrane of cells in the distal convoluted tubule. - This inhibition leads to decreased reabsorption of sodium and chloride, resulting in increased excretion of water, sodium, and chloride. *Proximal Convoluted Tubule* - The proximal convoluted tubule is the primary site for reabsorption of the majority of filtered substances, including sodium, bicarbonate, glucose, and amino acids. - While some diuretics like **acetazolamide** (a carbonic anhydrase inhibitor) act here, thiazides do not. *Glomerulus* - The **glomerulus** is primarily responsible for the **filtration** of blood, forming the initial filtrate. - It is not a site for diuretic action as it does not participate in active reabsorption or secretion of electrolytes. *Descending limb of loop of Henle* - The descending limb is highly permeable to **water** but impermeable to solutes, leading to water reabsorption due to the hyperosmotic medulla. - Diuretics typically do not act on this segment to inhibit solute transport, though osmotic diuretics can affect water movement here.
Question 87: What are the primary mechanisms behind cardiac toxicity associated with Tricyclic antidepressants?
- A. Norepinephrine reuptake inhibition only
- B. Anticholinergic effects on the heart
- C. Both norepinephrine reuptake inhibition and anticholinergic effects on the heart (Correct Answer)
- D. Direct membrane stabilizing effects only
Explanation: ***Both norepinephrine reuptake inhibition and anticholinergic effects on the heart*** - **Tricyclic antidepressants (TCAs)** block the reuptake of **norepinephrine**, which can lead to increased sympathetic tone on the heart and potentially **tachyarrhythmias** or other cardiac complications. - TCAs also have potent **anticholinergic effects**, blocking muscarinic receptors in the heart; this can increase **heart rate** and affect cardiovascular stability. - While **direct membrane stabilizing effects** (sodium channel blockade) are critical for **QRS widening and conduction delays**, the combination of norepinephrine reuptake inhibition and anticholinergic effects accounts for the broader spectrum of **TCA-induced cardiac toxicity** including tachycardia and hemodynamic instability. *Norepinephrine reuptake inhibition only* - While TCAs do inhibit norepinephrine reuptake contributing to tachycardia and increased sympathetic tone, this mechanism alone does not fully explain the breadth of cardiac effects seen with these drugs. - The **anticholinergic effects** play a significant additional role in altering cardiac function. *Anticholinergic effects on the heart* - While TCAs do exert anticholinergic effects that can impact heart rate and cardiovascular function, this mechanism alone fails to account for the additional contributions from **norepinephrine reuptake inhibition** to the overall cardiac toxicity. - The combination of both mechanisms is necessary for a complete understanding of **TCA-induced cardiac effects**. *Direct membrane stabilizing effects only* - This option refers to the **quinidine-like action** of TCAs, which involves blocking myocardial fast sodium channels, leading to a **prolonged QRS interval** and increased risk of **ventricular arrhythmias** and **conduction defects**. - While direct membrane stabilization is the **primary mechanism of TCA-induced conduction abnormalities** (QRS widening, heart blocks), the question asks for mechanisms of broader **cardiac toxicity**, which includes the combined effects of norepinephrine reuptake inhibition and anticholinergic actions on heart rate and hemodynamics.
Question 88: Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?
- A. Diazepam
- B. Zolpidem
- C. Phenobarbitone
- D. Buspirone (Correct Answer)
Explanation: ***Buspirone*** - **Buspirone** is a unique anxiolytic that primarily acts as a **partial agonist at 5-HT1A receptors**. - Unlike benzodiazepines, it lacks significant **anticonvulsant**, **muscle relaxant**, or **sedative-hypnotic properties** and does not lead to physical dependence or withdrawal. *Diazepam* - **Diazepam** is a **benzodiazepine** that acts by enhancing the effect of **GABA** at GABA-A receptors, leading to significant anxiolytic, sedative, muscle relaxant, and anticonvulsant effects. - It does not primarily act via **5-HT1A receptor partial agonism**. *Zolpidem* - **Zolpidem** is a **non-benzodiazepine hypnotic** that selectively binds to the **GABA-A receptor** subunit, primarily mediating sedative effects. - While it's used for insomnia, it doesn't primarily act as a **5-HT1A partial agonist** and is not typically used for its anxiolytic properties in the same way as buspirone. *Phenobarbitone* - **Phenobarbitone** is a **barbiturate** that acts by prolonging the opening of **chloride channels** associated with GABA-A receptors, leading to strong sedative, hypnotic, and anticonvulsant effects. - Its mechanism of action is distinct from **5-HT1A receptor partial agonism**, and it carries a high risk of dependence and overdose.
Question 89: Lithium directly affects which ion ?
- A. Sodium (Correct Answer)
- B. Potassium
- C. Magnesium
- D. Calcium
Explanation: ***Sodium*** - Lithium directly interferes with **sodium ion transport** across cell membranes, particularly by inhibiting the **Na+/K+-ATPase** pump. - This interference alters intracellular sodium concentrations and affects neural excitability, contributing to its **mood-stabilizing** effects. *Potassium* - While potassium transport is linked to the **Na+/K+-ATPase pump**, lithium primarily acts through its effect on **sodium transport**, rather than directly mimicking or significantly altering potassium. - Changes in potassium levels due to lithium are largely secondary to its primary impact on sodium. *Magnesium* - Lithium has a more direct impact on **sodium channels** and transporters, contrasting with its less direct or significant interaction with magnesium metabolism. - Though magnesium is crucial for numerous cellular processes, it is not the primary ion directly affected by lithium's therapeutic actions. *Calcium* - Lithium does not directly affect **calcium channels** or calcium signaling pathways in the same way it impacts sodium. - While lithium may indirectly influence calcium-dependent processes, its primary direct target for therapeutic effects is not calcium.
Question 90: Which of the following is a classic tricyclic antidepressant (TCA) commonly used as the prototype for the class?
- A. Amitriptyline (Correct Answer)
- B. Citalopram
- C. Venlafaxine
- D. Nortriptyline
Explanation: ***Amitriptyline*** - **Amitriptyline** is a classic tricyclic antidepressant (TCA) and is widely recognized for its use in treating depression, neuropathic pain, and migraine prophylaxis. Its characteristic side effect profile, including **anticholinergic effects** and **sedation**, is well-known. - It is one of the **oldest and most frequently prescribed TCAs**, making it a common reference point in pharmacology and clinical practice. *Citalopram* - **Citalopram** is an **SSRI** (selective serotonin reuptake inhibitor), not a TCA. It works by selectively inhibiting the reuptake of serotonin. - It has a different side effect profile compared to TCAs, generally with fewer anticholinergic and cardiovascular effects. *Venlafaxine* - **Venlafaxine** is an **SNRI** (serotonin-norepinephrine reuptake inhibitor), not a TCA. It inhibits the reuptake of both serotonin and norepinephrine. - It has efficacy in treating depression and anxiety disorders, but its mechanism of action is distinct from TCAs. *Nortriptyline* - **Nortriptyline** is indeed a TCA, specifically a **secondary amine TCA**, which is an active metabolite of amitriptyline. - While it is a TCA, amitriptyline is generally more broadly recognized and used as the prototype for the class, with nortriptyline often being highlighted for its slightly better tolerability profile (e.g., less sedation, less orthostatic hypotension) compared to tertiary amine TCAs like amitriptyline.