NEET-PG 2013 - Pharmacology Practice Questions

Q: Aminophylline inhibits which of the following enzymes?

Phosphodiesterase. ***Phosphodiesterase*** - **Aminophylline** is a methylxanthine derivative that primarily acts as a **phosphodiesterase (PDE) inhibitor** [1], [2]. - By inhibiting PDE, aminophylline increases intracellular levels of **cAMP** and **cGMP**, leading to **bronchodilation** and other effects [2], [3]. *MAO* - **MAO (monoamine oxidase)** inhibitors are antidepressants that prevent the breakdown of neurotransmitters like serotonin, norepinephrine, and dopamine. - Aminophylline does not significantly inhibit MAO. *Alcohol dehydrogenase* - **Alcohol dehydrogenase** is an enzyme responsible for metabolizing alcohol (ethanol) in the liver. - Aminophylline has no direct inhibitory effect on alcohol dehydrogenase. *Cytochrome P450* - **Cytochrome P450 (CYP450)** enzymes are a group of enzymes primarily involved in the metabolism of drugs and other xenobiotics in the liver [4]. - While aminophylline (and its active metabolite theophylline) can be metabolized by and *affect* certain **CYP450** isoenzymes (e.g., CYP1A2), it does not act as a general inhibitor of the entire CYP450 system; its primary therapeutic action is not through CYP450 inhibition.

Q: Which of the following is NOT a beta-2 agonist?

Ketotifen. ***Ketotifen*** - **Ketotifen** is an **oral anti-allergic drug** that acts as a **mast cell stabilizer** and **H1-antihistamine**, not a beta-2 agonist. - It is used for **prophylactic treatment** of asthma and allergic conditions, working through different mechanisms than bronchodilators. *Terbutaline* - **Terbutaline** is a **short-acting beta-2 agonist (SABA)** used for bronchodilation in asthma and COPD [2]. - Available in **oral, inhaled, and injectable forms** for rapid relief of bronchospasm. *Salbutamol* - **Salbutamol** (also known as albuterol) is a **short-acting beta-2 agonist (SABA)** and the most widely used rescue inhaler for asthma [1], [2]. - Provides **rapid bronchodilation** by stimulating beta-2 receptors in airway smooth muscles [3]. *Bambuterol* - **Bambuterol** is a **long-acting beta-2 agonist (LABA)** that is a prodrug of **terbutaline**. - It is slowly converted to the active form in the body, providing **sustained bronchodilation** for maintenance therapy.

Q: Beta2-agonists cause all except:

Hyperkalemia. ***Hyperkalemia*** - Beta2-agonists actually cause **hypokalemia**, not hyperkalemia, by promoting the intracellular shift of potassium. - This effect is due to the stimulation of the **Na+/K+-ATPase pump** by beta-2 adrenergic receptors. *Hyperglycemia* - Beta2-agonists can lead to **hyperglycemia** by promoting glycogenolysis and gluconeogenesis in the liver. - They also decrease **insulin secretion** and increase insulin resistance. *Tremor* - **Tremor** is a common side effect of beta2-agonists, particularly in the hands, due to direct stimulation of beta2 receptors on skeletal muscle. - This muscle stimulation leads to increased muscle twitching and a fine tremor. *Palpitation* - **Palpitations** can occur due to the systemic absorption of beta2-agonists, leading to activation of beta1 receptors in the heart. - This can cause **tachycardia** and a sensation of a racing heart.

Q: What is the mechanism of action of Abatacept?

Inhibitor of co-stimulation of T cells. ***Inhibitor of co-stimulation of T cells*** - Abatacept is a **fusion protein** that blocks the **CD28-CD80/86 co-stimulatory pathway**, which is crucial for full T-cell activation. - By binding to **CD80** and **CD86** on antigen-presenting cells, it prevents their interaction with **CD28** on T cells, thus inhibiting T-cell proliferation and cytokine production. *Tumor necrosis factor (TNF) alpha inhibitor* - TNF alpha inhibitors (e.g., **adalimumab**, **infliximab**, **etanercept**) bind to and neutralize **TNF alpha**, a pro-inflammatory cytokine. - While used in similar conditions, their mechanism is distinct from Abatacept's T-cell co-stimulation blockade. *Monoclonal antibody against interleukin-6 (IL-6) receptor* - Drugs like **tocilizumab** target the **IL-6 receptor**, blocking the signaling of **IL-6**, another important inflammatory cytokine. - This mechanism primarily affects cytokine signaling rather than directly inhibiting T-cell activation in the same way as abatacept. *Interleukin-1 (IL-1) receptor antagonist* - **Anakinra** is an example of an **IL-1 receptor antagonist**, which competes with IL-1 for binding to its receptor, thereby blocking its pro-inflammatory effects. - This mechanism focuses on inhibiting the action of IL-1, unlike Abatacept's role in T-cell activation.

Q: Why do NSAIDs cause gastric ulcers?

They inhibit COX-1 and COX-2 enzymes. ***They inhibit COX-1 and COX-2 enzymes*** - NSAIDs primarily exert their anti-inflammatory effects by inhibiting **cyclooxygenase (COX) enzymes**, specifically COX-1 and COX-2. - While COX-2 inhibition is responsible for anti-inflammatory action, **COX-1 inhibition** reduces the production of protective prostaglandins in the gastric mucosa, leading to a loss of mucosal integrity and an increased risk of ulceration. *They inhibit the production of protective mucus* - While NSAIDs do compromise the gastric mucosal barrier, their primary mechanism is not a direct inhibition of mucus production itself. - Instead, the reduced prostaglandin synthesis indirectly affects the quantity and quality of mucus and bicarbonate, which are crucial for mucosal defense. *They increase gastric acid secretion* - NSAIDs do not directly increase gastric acid secretion; in fact, some studies suggest a mild inhibitory effect. - The main problem is the diminished mucosal protection against the normal levels of gastric acid. *They delay gastric emptying* - Delaying gastric emptying is not a primary mechanism by which NSAIDs cause ulcers. - While some medications can affect gastric motility, this is not the key pathway for NSAID-induced gastropathy.

Q: Which of the following is a mineralocorticoid antagonist?

Spironolactone. ***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.

Q: Thiazides act on which part of the nephron?

Distal Convoluted Tubule. ***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.

Q: Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?

Buspirone. ***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.

Q: Lithium directly affects which ion ?

Sodium. ***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 1

Aminophylline inhibits which of the following enzymes?

Accepted Answer

Phosphodiesterase

Answer

MAO

Answer

Alcohol dehydrogenase

Answer

Cytochrome P450

Question 2

Which of the following is NOT a beta-2 agonist?

Accepted Answer

Ketotifen

Answer

Terbutaline

Answer

Salbutamol

Answer

Bambuterol

Question 3

Beta2-agonists cause all except:

Accepted Answer

Hyperkalemia

Answer

Hyperglycemia

Answer

Tremor

Answer

Palpitation

Question 4

What is the mechanism of action of Abatacept?

Accepted Answer

Inhibitor of co-stimulation of T cells

Answer

Tumor necrosis factor (TNF) alpha inhibitor

Answer

Monoclonal antibody against interleukin-6 (IL-6) receptor

Answer

Interleukin-1 (IL-1) receptor antagonist

Question 5

Why do NSAIDs cause gastric ulcers?

Accepted Answer

They inhibit COX-1 and COX-2 enzymes

Answer

They increase gastric acid secretion

Answer

They delay gastric emptying

Answer

They inhibit the production of protective mucus

Question 6

Which of the following is a mineralocorticoid antagonist?

Accepted Answer

Spironolactone

Answer

Inamrinone

Answer

Nicorandil

Answer

Ketorolac

Question 7

Thiazides act on which part of the nephron?

Accepted Answer

Distal Convoluted Tubule

Answer

Proximal Convoluted Tubule

Answer

Descending limb of loop of Henle

Answer

Glomerulus

Question 8

What are the primary mechanisms behind cardiac toxicity associated with Tricyclic antidepressants?

Accepted Answer

Both norepinephrine reuptake inhibition and anticholinergic effects on the heart

Answer

Norepinephrine reuptake inhibition only

Answer

Anticholinergic effects on the heart

Answer

Direct membrane stabilizing effects only

Question 9

Which anxiolytic acts through 5-HT1A receptor partial agonism without exhibiting significant anticonvulsant or muscle relaxant properties?

Accepted Answer

Buspirone

Answer

Diazepam

Answer

Zolpidem

Answer

Phenobarbitone

Question 10

Lithium directly affects which ion ?

Accepted Answer

Sodium

Answer

Potassium

Answer

Magnesium

Answer

Calcium

NEET-PG 2013 — Pharmacology