General Pharmacology — MCQs

General Pharmacology Indian Medical PG Practice Questions and MCQs

Question 641: Which of the following statements is true about atosiban?

A. is an oxytocin receptor antagonist (Correct Answer)
B. is least effective in inhibiting preterm uterine contractions
C. is a progesterone receptor antagonist
D. acts primarily on beta-adrenergic receptors

Explanation: ***is an oxytocin receptor antagonist*** - **Atosiban** works by competitively binding to **oxytocin receptors** in the myometrium, thereby preventing oxytocin from stimulating uterine contractions. - This action makes it effective in delaying **preterm labor** by reducing the frequency and intensity of contractions. - Atosiban is classified as a **tocolytic drug** specifically because of its oxytocin receptor antagonism. *is least effective in inhibiting preterm uterine contractions* - **Atosiban** is an **effective tocolytic** used to delay preterm labor, making this statement incorrect. - Studies show it can prolong pregnancy for several days, allowing for the administration of **corticosteroids** for fetal lung maturation. *is a progesterone receptor antagonist* - **Atosiban** specifically targets **oxytocin receptors**, not progesterone receptors. - Progesterone receptor antagonists (e.g., **mifepristone**) would induce labor rather than suppress it. *acts primarily on beta-adrenergic receptors* - **Atosiban** does not act on beta-adrenergic receptors; it is an **oxytocin receptor antagonist**. - Beta-adrenergic agonists like **ritodrine** and **terbutaline** are different tocolytics that work by relaxing uterine smooth muscle through beta-2 receptor stimulation.

Question 642: What is the classification of Sumatriptan?

A. 5HT 1B/1D agonist (Correct Answer)
B. 5HT 1D antagonist
C. 5HT 1A antagonist
D. 5HT 1 agonist

Explanation: ***5HT 1B/1D agonist*** - Sumatriptan is a **selective serotonin receptor agonist**, specifically targeting the **5-HT1B** and **5-HT1D** receptor subtypes. - This is the **precise pharmacological classification** of triptans used in acute migraine treatment. - Agonism at **5-HT1B receptors** causes **vasoconstriction** of dilated cranial blood vessels. - Agonism at **5-HT1D receptors** inhibits the release of **pro-inflammatory neuropeptides** (CGRP, substance P) from trigeminal nerve endings. - This specific classification distinguishes sumatriptan from non-selective serotonin agonists. *5HT 1 agonist* - While technically not incorrect, this classification is **too broad and imprecise** for pharmacological purposes. - A general "5-HT1 agonist" could theoretically include activity at 5-HT1A, 1B, 1D, 1E, and 1F receptors. - Sumatriptan has **minimal affinity** for 5-HT1A receptors and its therapeutic effect is specifically due to 5-HT1B/1D activity. - In medical literature and standard pharmacology texts, triptans are classified as **5-HT1B/1D agonists**, not general 5-HT1 agonists. *5HT 1D antagonist* - An **antagonist** blocks receptor activity rather than activating it. - This would **worsen** migraine symptoms by preventing the therapeutic effects of endogenous serotonin. - There are no established antimigraine drugs that act as 5-HT1D antagonists. *5HT 1A antagonist* - 5-HT1A receptors are primarily involved in **mood regulation, anxiety, and sleep**, not acute migraine pathophysiology. - Sumatriptan has minimal activity at 5-HT1A receptors. - Antagonism at this receptor would not provide antimigraine effects and is unrelated to sumatriptan's mechanism.

Question 643: Hypercalcemia is caused by all except:

A. Lithium
B. Loop diuretics (Correct Answer)
C. Thiazides
D. Vitamin D intoxication

Explanation: Hypercalcemia is caused by all except: ***Loop diuretics*** - **Loop diuretics** promote the urinary excretion of calcium by inhibiting the reabsorption of calcium in the thick ascending limb of the loop of Henle [3]. - This effect leads to a **decrease** in serum calcium levels and thus do not cause hypercalcemia. [3] *Lithium* - **Lithium** can cause hypercalcemia by increasing the set point for calcium sensing in the parathyroid glands, leading to increased parathyroid hormone (PTH) secretion. - This results in a mild, chronic hypercalcemia, often in the context of **secondary hyperparathyroidism**. *Vitamin D intoxication* - **Vitamin D intoxication** leads to excessive absorption of calcium from the gut and increased bone resorption, both contributing to hypercalcemia [1]. - High levels of vitamin D cause hypercalcemia that **suppresses PTH secretion** through negative feedback, resulting in hypercalcemia with inappropriately low PTH levels. *Thiazides* - **Thiazide diuretics** can cause mild hypercalcemia by increasing renal tubular reabsorption of calcium [2]. - They enhance calcium reabsorption in the **distal convoluted tubule**, leading to a slight elevation in serum calcium [2], [3].

Question 644: Which one of the following drugs does not interfere with folic acid metabolism?

A. Phenobarbitone
B. Primidone
C. Gabapentin (Correct Answer)
D. Phenytoin

Explanation: ***Gabapentin*** - **Gabapentin** is an anticonvulsant that primarily exerts its effects by modulating activity at voltage-gated calcium channels; it does **not interfere with folic acid metabolism**. - Its mechanism of action is distinct from other antiepileptic drugs that are known to cause folate deficiency. *Phenobarbitone* - **Phenobarbitone** is an antiepileptic drug that belongs to the barbiturate class and is known to be an **inducer of hepatic microsomal enzymes**. - This enzyme induction can **increase the metabolism of folic acid**, leading to its depletion and potentially megaloblastic anemia. *Primidone* - **Primidone** is an antiepileptic drug that is metabolized to **phenobarbitone** and phenylethylmalonamide (PEMA). - Like phenobarbitone, it is an **hepatic enzyme inducer** and can therefore **interfere with folic acid metabolism**. *Phenytoin* - **Phenytoin** is a well-known antiepileptic drug that often causes **folate deficiency**. - It interferes with folate metabolism by **inhibiting intestinal folate absorption** and by increasing its breakdown through enzyme induction.

Question 645: Suxamethonium is available as a clear, colourless aqueous solution. What is the shelf life of suxamethonium when stored correctly?

A. 1 year
B. 3 years
C. 2 years (Correct Answer)
D. 6 months

Explanation: ***2 years*** - When **stored correctly** (refrigerated between 2-8°C and protected from light), the typical shelf life of suxamethonium is **2 years**. [1] - This stability ensures its effectiveness as a **neuromuscular blocking agent** when needed for medical procedures. [1] *6 months* - A 6-month shelf life is generally too short for the refrigerated, unopened vials of **suxamethonium** from the manufacturer. - This period is more commonly associated with the stability of certain reconstituted or diluted medications. *1 year* - While some medications might have a 1-year shelf life, **suxamethonium** typically has a longer stability period when stored under optimal conditions. - A 1-year shelf life would be relatively short for an unopened, stock solution of this drug. *3 years* - A 3-year shelf life is generally considered too long for **suxamethonium** under standard refrigerated storage conditions. - Most manufacturers specify a 2-year shelf life to maintain drug efficacy and safety.

Question 646: Which of the following describes the type of measles vaccine used in immunization?

A. The vaccine is given in two doses.
B. It provides lifelong immunity.
C. It is a live attenuated vaccine. (Correct Answer)
D. The vaccine is typically administered at 12 months of age.

Explanation: ***It is a live attenuated vaccine.*** - The **measles vaccine** contains a weakened form of the measles virus, allowing it to replicate in the body without causing disease. - This type of vaccine elicits a strong, **long-lasting immune response** resembling natural infection. - Live attenuated vaccines are preferred for measles because they provide superior cellular and humoral immunity compared to inactivated vaccines. *It provides lifelong immunity.* - While the measles vaccine provides **long-lasting and robust immunity**, it is not always lifelong for everyone, and a second dose is recommended to ensure maximal protection. - Immunity can wane over time in some individuals, making them susceptible to infection. - This describes the vaccine's **effectiveness**, not its type or composition. *The vaccine is given in two doses.* - The standard measles vaccination schedule involves **two doses**, typically given as part of the MMR (measles, mumps, rubella) vaccine. - This describes the **administration protocol**, not the vaccine type itself. *The vaccine is typically administered at 12 months of age.* - The **first dose** of the measles vaccine (MMR) is commonly administered between **12 and 15 months of age**, with the second dose between 4 and 6 years. - This timing describes the **administration schedule**, not the vaccine type or composition.

Question 647: What is the primary mechanism by which steroids exert their anti-inflammatory action?

A. Phospholipase A2 (Correct Answer)
B. Myeloperoxidase
C. Cyclooxygenase
D. Lipoxygenase

Explanation: ***Phospholipase A2*** - Steroids exert their primary anti-inflammatory action by inducing the synthesis of **lipocortin-1 (annexin-1)**, which then inhibits **phospholipase A2 (PLA2)**, an enzyme crucial for the release of **arachidonic acid** from cell membrane phospholipids. - By blocking PLA2, steroids prevent the formation of all subsequent inflammatory mediators derived from arachidonic acid, including **prostaglandins**, **leukotrienes**, and **thromboxanes**. - This represents the most **upstream** mechanism of steroid anti-inflammatory action, affecting multiple downstream pathways simultaneously. *Cyclooxygenase* - **Cyclooxygenase (COX)** enzymes, specifically COX-1 and COX-2, are responsible for converting arachidonic acid into **prostaglandins** and **thromboxanes**. - While steroids ultimately reduce COX activity by limiting substrate availability, their direct and primary inhibition is not on COX itself but at an earlier step in the inflammatory cascade. *Lipoxygenase* - The **lipoxygenase (LOX)** pathway converts arachidonic acid into **leukotrienes**, which are potent mediators of inflammation, particularly in asthma and allergic reactions. - Steroids do inhibit the formation of leukotrienes indirectly by blocking their precursor, arachidonic acid, but their direct target is not LOX itself. *Myeloperoxidase* - **Myeloperoxidase** is an enzyme found primarily in **neutrophils** and macrophages, playing a role in oxidative stress and microbial killing by producing hypochlorous acid (bleach). - While steroids can modulate immune cell function, their direct anti-inflammatory mechanism is not through the inhibition of myeloperoxidase activity.

Question 648: What does the therapeutic index of a drug signify?

A. Dose which produces maximum effect
B. Safety margin (Correct Answer)
C. Efficacy
D. Maximum response that can be elicited by a drug

Explanation: ***Safety margin*** - The **therapeutic index (TI)** is a ratio comparing the dose that produces a toxic effect (TD50 or LD50) to the dose that produces a therapeutically desired effect (ED50) [1]. - A higher therapeutic index indicates a **wider safety margin**, meaning there is a greater difference between the effective and toxic doses [1, 2].*Dose which produces maximum effect* - This describes the **efficacy** of a drug at its maximal point, not its therapeutic index. - The therapeutic index is concerned with the range of doses that can be safely given to achieve a therapeutic effect [2].*Efficacy* - **Efficacy** refers to the maximum effect a drug can produce regardless of the dose. - The therapeutic index is a measure of drug safety, not primarily its efficacy [1].*Maximum response that can be elicited by a drug* - This definition also describes the **efficacy** or **maximal effect** of a drug. - The therapeutic index quantifies the **ratio of toxic to effective doses**, providing insight into safety [1].

Question 649: All of the following are adverse effects of glucocorticoids except:

A. Peptic ulcer
B. Infections
C. Hypoglycemia (Correct Answer)
D. Cataract

Explanation: ***Hypoglycemia*** - Glucocorticoids are known to **increase blood glucose levels** by promoting gluconeogenesis and glycogenolysis, thus they cause **hyperglycemia**, not hypoglycemia. - They also induce **insulin resistance**, further contributing to elevated blood sugar. *Cataract* - Long-term use of high-dose glucocorticoids can cause **posterior subcapsular cataracts** due to metabolic changes in the lens. - This is a well-recognized ocular side effect of corticosteroids. *Peptic ulcer* - Glucocorticoids can impair the **gastric mucosal barrier**, increase acid secretion, and reduce prostaglandin synthesis, leading to an increased risk of **peptic ulcers**. - This effect is potentiated when used concurrently with NSAIDs. *Infections* - Glucocorticoids are **immunosuppressive**, reducing the body's ability to fight off pathogens. - This increases susceptibility to various infections, including bacterial, viral, fungal, and opportunistic infections.

Question 650: Therapeutic index of a drug is an indicator of its:

A. Effectiveness
B. Adverse Effects
C. Therapeutic Effect
D. Safety Profile (Correct Answer)

Explanation: ***Safety Profile*** - The **therapeutic index (TI)** is a ratio that compares the dose of a drug that produces a **toxic effect** to the dose that produces a **therapeutically desired effect**. - A higher therapeutic index generally indicates a **safer drug**, as it means a larger dose is required to cause toxic effects compared to the therapeutic dose. *Effectiveness* - While related to efficacy, effectiveness usually refers to how well a drug works in **real-world clinical practice**, not directly measured by the therapeutic index. - The therapeutic index focuses on the **margin between efficacy and toxicity**, rather than just the degree of positive response. *Adverse Effects* - The **therapeutic index** considers the toxic dose, which leads to adverse effects, but it's a measure of the **margin of safety**, not just the presence or absence of adverse effects. - It quantifies the **risk of adverse effects** relative to the therapeutic benefit, rather than simply listing or describing them. *Therapeutic Effect* - The **therapeutic index** incorporates the dose required for a therapeutic effect, but its primary purpose is to assess the **risk of toxicity** in relation to that therapeutic effect. - It's a measure of the **balance between benefit and harm**, not solely the therapeutic benefit itself.

Practice by Chapter

Pharmacokinetics: Absorption and Distribution

Practice Questions

Pharmacokinetics: Metabolism and Excretion

Practice Questions

Pharmacodynamics and Receptor Theory

Practice Questions

Drug-Receptor Interactions and Dose-Response

Practice Questions

Pharmacogenetics and Personalized Medicine

Practice Questions

Adverse Drug Reactions and Toxicity

Practice Questions

Drug Interactions

Practice Questions

Drug Development and Regulation

Practice Questions

Pediatric and Geriatric Pharmacology

Practice Questions

Placental Transfer and Lactation

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free