General Pharmacology — MCQs

General Pharmacology Indian Medical PG Practice Questions and MCQs

Question 621: Fenfluramine was historically used for which condition before its withdrawal from the market?

A. Malignancy
B. Obesity (Correct Answer)
C. Diabetes mellitus
D. Hypertension

Explanation: ***Obesity*** - Fenfluramine was notably used as an **anorectic agent** (appetite suppressant) for the treatment of **obesity** - Often prescribed in combination with phentermine, known as **"fen-phen"** - The drug was effective in promoting **weight loss** through its mechanism as a **serotonergic agent** that enhanced satiety - It was **withdrawn from the market in 1997** due to associations with **valvular heart disease** and **pulmonary hypertension**, not due to lack of efficacy *Malignancy* - Fenfluramine has **never been approved** or used for the treatment of **malignancy** or cancer - There is no historical or clinical data supporting its use as an anticancer agent - Its mechanism of action is related to appetite suppression, not cancer treatment *Hypertension* - Fenfluramine was **not used to treat hypertension** - Ironically, it was associated with **causing pulmonary hypertension** as a serious adverse effect - Its mechanism as a serotonergic agent for appetite suppression is unrelated to systemic blood pressure control *Diabetes mellitus* - Fenfluramine was not indicated for **diabetes mellitus** treatment - While weight loss can improve glycemic control, fenfluramine was specifically marketed as an **anti-obesity medication**, not an antidiabetic drug

Question 622: What is the primary mechanism of action of Apremilast?

A. Inhibition of IL-17
B. Inhibition of CD25
C. Inhibition of PDE-4 (Correct Answer)
D. Inhibition of IL-23

Explanation: ***Inhibition of PDE-4*** - **Apremilast** is a small molecule inhibitor specifically targeting **phosphodiesterase 4 (PDE4)**. - By inhibiting PDE4, Apremilast increases intracellular levels of **cyclic adenosine monophosphate (cAMP)**, leading to a modulation of pro-inflammatory and anti-inflammatory mediators. *Inhibition of IL-17* - This mechanism is primarily associated with biologics like **secukinumab** and **ixekizumab**, which are monoclonal antibodies that directly block IL-17A. - While IL-17 is involved in inflammatory conditions treated by Apremilast, Apremilast does not directly inhibit IL-17 itself. *Inhibition of CD25* - **CD25** is the alpha subunit of the **IL-2 receptor**, and its inhibition (e.g., by basiliximab) is primarily used for **immunosuppression** in organ transplantation to prevent T-cell activation. - This mechanism is not related to the action of Apremilast. *Inhibition of IL-23* - This mechanism is characteristic of biologics such as **guselkumab**, **risankizumab**, and **tildrakizumab**, which target the p19 subunit of **IL-23**. - These drugs are used in conditions like psoriasis, but their mechanism differs from Apremilast's PDE4 inhibition.

Question 623: The drug of choice in motion sickness is:

A. Hyoscine (Correct Answer)
B. Domperidone
C. Promethazine
D. Metoclopramide

Explanation: ***Hyoscine*** - **Hyoscine (scopolamine)** is an **anticholinergic** agent that acts by blocking muscarinic receptors in the vestibular system and the vomiting center. - It is highly effective for preventing and treating **motion sickness**, particularly when administered transdermally or orally before travel. *Domperidone* - **Domperidone** is a **D2 dopamine receptor antagonist** that acts peripherally to increase gastric motility and reduce nausea. - It is primarily used for **gastroparesis** and **nausea/vomiting** caused by gastrointestinal issues or dopamine agonist drugs, but it is not the first-line choice for motion sickness due to limited central nervous system penetration. *Promethazine* - **Promethazine** is an **H1 antihistamine** with significant anticholinergic and sedative properties. - While it can be used for motion sickness due to its **sedative effects** and action on the vomiting center, it is generally considered a second-line option due to pronounced drowsiness, and **hyoscine** is more potent specifically for motion sickness. *Metoclopramide* - **Metoclopramide** is a **D2 dopamine receptor antagonist** both centrally and peripherally, which increases gastric emptying and possesses antiemetic properties. - It is effective for **nausea and vomiting** associated with gastroparesis, migraines, or chemotherapy, but is less effective for motion sickness as its primary mechanism of action does not directly target the vestibular input pathways as effectively as hyoscine.

Question 624: Which of the following is a Rho kinase inhibitor?

A. Fasudil (Correct Answer)
B. Ranolazine
C. Amiloride
D. Nicorandil

Explanation: ***Fasudil*** - **Fasudil** is a well-known and clinically used **Rho kinase inhibitor**, primarily used in Japan for the treatment of **cerebral vasospasm** after subarachnoid hemorrhage. - It works by inhibiting the phosphorylation of **myosin light chain**, leading to **vasodilation**. *Ranolazine* - **Ranolazine** is an anti-anginal drug that works by selectively inhibiting the **late sodium current (I_Na)** in cardiac myocytes. - This reduces intracellular sodium and calcium overload, thereby improving myocardial relaxation and reducing oxygen demand, but it has no direct inhibitory effect on Rho kinase. *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that directly inhibits the **epithelial sodium channel (ENaC)** in the collecting duct. - It is used to treat **hypertension** and heart failure, preventing potassium loss, and is not associated with Rho kinase inhibition. *Nicorandil* - **Nicorandil** is an anti-anginal drug with a dual mechanism, acting as both a **potassium channel opener** and a **nitrate donor**. - Its vasodilatory effects are mediated through increasing cGMP (like nitrates) and hyperpolarizing vascular smooth muscle cells (like potassium channel openers), but it is not a Rho kinase inhibitor.

Question 625: Among NSAIDs, aspirin is unique because it:

A. Irreversibly inhibits its target enzyme (Correct Answer)
B. Reduces fever
C. Selectively inhibits COX-1 enzyme
D. May reduce the risk of colon cancer

Explanation: ***Irreversibly inhibits its target enzyme*** - Aspirin uniquely acetylates a **serine residue** on both **COX-1 and COX-2**, permanently inactivating the enzyme. - This irreversible inhibition is why aspirin's antiplatelet effects last for the lifespan of the platelet (7-10 days), unlike other NSAIDs which are reversible inhibitors. *May reduce the risk of colon cancer* - While some studies suggest a link between long-term aspirin use and reduced colon cancer risk, this is a property shared by some other NSAIDs and is not a unique distinguishing feature of aspirin among NSAIDs. - This effect is generally attributed to the **inhibition of COX-2**, which is involved in tumor growth and inflammation. *Reduces fever* - **Antipyresis** (fever reduction) is a characteristic effect of nearly all NSAIDs, including ibuprofen and naproxen, due to the inhibition of prostaglandin synthesis in the hypothalamus. - Therefore, this is not a unique feature of aspirin. *Selectively inhibits COX-1 enzyme* - Aspirin is a **non-selective COX inhibitor**, meaning it inhibits both COX-1 and COX-2 enzymes at anti-inflammatory doses. - While it has a higher affinity for COX-1 at low doses, drugs like celecoxib are genuinely selective COX-2 inhibitors, and no common NSAID is purely selective for COX-1.

Question 626: Which group of afferent fibers is most sensitive to local anesthetics?

A. Group A fibers
B. Group B fibers (Correct Answer)
C. Group C fibers
D. Group D fibers

Explanation: ***Group B fibers***- These are **small, myelinated preganglionic autonomic fibers** that are the **MOST sensitive** to local anesthetics [1].- Their **small diameter combined with myelination** makes them highly susceptible to blockade at the **nodes of Ranvier**.- The classic order of sensitivity is: **B > C > A-delta > A-gamma > A-beta > A-alpha** [1].*Group C fibers*- These are **unmyelinated, small-diameter fibers** transmitting **dull pain and temperature** sensations.- They are the **second most sensitive** to local anesthetics after B fibers.- While their small diameter makes them susceptible, the lack of myelination means blockade occurs more slowly than in B fibers.*Group A fibers*- This group includes **large-diameter, myelinated fibers** (A , A , A , A ) transmitting motor, proprioception, touch, and sharp pain signals.- Their **larger diameter** provides **greater resistance** to local anesthetic blockade.- A-delta fibers (sharp pain) are more sensitive than other A fibers but still less sensitive than B and C fibers.*Group D fibers*- There is **no standard "Group D"** fiber classification in neurophysiology.- The standard classifications are **A (alpha, beta, gamma, delta), B, and C fibers** based on diameter and myelination status.

Question 627: Which of the following local anesthetic agents is a vasoconstrictor?

A. Lignocaine
B. Cocaine (Correct Answer)
C. Bupivacaine
D. Tetracaine

Explanation: ***Cocaine*** - Cocaine is unique among local anesthetics as it is a potent **vasoconstrictor**, inhibiting **norepinephrine reuptake** at nerve terminals. - This vasoconstrictive property reduces bleeding and prolongs its anesthetic effect, but also contributes to its cardiotoxicity. *Lignocaine* - Lignocaine (Lidocaine) is an **amide-type local anesthetic** that causes **vasodilation**, which can lead to increased systemic absorption and a shorter duration of action [1]. - Due to its vasodilatory effect, **epinephrine** is often added to lignocaine to limit systemic absorption, prolong its effect, and reduce bleeding [1]. *Bupivacaine* - Bupivacaine is a long-acting **amide-type local anesthetic** that typically causes **vasodilation**, similar to lignocaine. - Its high potency and long duration of action make it suitable for local infiltrations and epidural anesthesia, but it also increases the risk of **cardiotoxicity** [1]. *Tetracaine* - Tetracaine is a potent and long-acting **ester-type local anesthetic** that also causes **vasodilation**. - It is primarily used for **spinal anesthesia** and topical applications and is usually combined with vasoconstrictors to prolong its effect.

Question 628: Which of the following medications is known to cause dysgeusia?

A. Captopril (Correct Answer)
B. Enalapril
C. Ramipril
D. Lisinopril

Explanation: ***Captopril*** - **Captopril**, an ACE inhibitor, is well-known for causing taste disturbances, specifically **dysgeusia** (altered taste sensation) or **ageusia** (loss of taste). - This side effect is thought to be related to its **sulfhydryl group** [1], which can chelate zinc, a metal crucial for normal taste perception. *Enalapril* - While also an ACE inhibitor, **enalapril** rarely causes taste disturbances compared to captopril. - It lacks the **sulfhydryl group** present in captopril, which is implicated in the mechanism of dysgeusia. *Ramipril* - **Ramipril** is another ACE inhibitor not commonly associated with dysgeusia. - Its chemical structure does not contain the **sulfhydryl group** that is linked to taste alterations. *Lisinopril* - **Lisinopril**, like enalapril and ramipril, is an ACE inhibitor that **seldom** causes dysgeusia. - The absence of the **sulfhydryl group** is a key differentiator from captopril regarding this specific side effect.

Question 629: Which opioid is MOST commonly available and used as a nasal spray formulation for acute pain management?

A. Tramadol
B. Butorphanol (Correct Answer)
C. Buprenorphine
D. Codeine

Explanation: ***Butorphanol*** - **Butorphanol** is a synthetic opioid agonist-antagonist that is **most commonly** available as a **nasal spray** formulation (Stadol NS), primarily used for the treatment of **migraines** and **moderate to severe acute pain**. - Its **intranasal formulation** allows for rapid absorption and quick onset of action, making it the **most widely prescribed** nasal opioid for acute pain relief. - It has been marketed as a nasal spray for decades and remains the **gold standard** intranasal opioid analgesic. *Tramadol* - **Tramadol** is an opioid analgesic typically available in **oral** (tablets, capsules) and **injectable** forms. - While some research has explored intranasal formulations, it is **not commercially available** as a nasal spray for routine pain management. *Codeine* - **Codeine** is a prodrug metabolized to morphine and is widely available in **oral formulations** (tablets, syrups) and sometimes in injectable forms. - It is **not available** as a nasal spray for pain relief. *Buprenorphine* - **Buprenorphine** is a partial opioid agonist available in various formulations including **sublingual tablets**, **transdermal patches**, and **injectable solutions**. - While buprenorphine **nasal spray formulations do exist** (primarily for opioid use disorder treatment), **butorphanol** remains the **most commonly used and prescribed** intranasal opioid specifically for **acute pain management**.

Question 630: What is the classification of the drug Anakinra?

A. IL-1 antagonist (Correct Answer)
B. IL-2 antagonist
C. IL-6 antagonist
D. IL-10 antagonist

Explanation: ***IL-1 antagonist*** - **Anakinra** is a recombinant form of the human **interleukin-1 receptor antagonist (IL-1Ra)**, which competitively inhibits the binding of IL-1 to its receptors. - By blocking IL-1, Anakinra reduces inflammation and tissue damage in conditions like **rheumatoid arthritis** and **systemic juvenile idiopathic arthritis**. *IL-2 antagonist* - **IL-2 antagonists** (e.g., basiliximab, daclizumab) are primarily used as **immunosuppressants** to prevent organ transplant rejection. - They act by blocking the action of **interleukin-2**, a cytokine crucial for T-cell proliferation and activation. *IL-6 antagonist* - **IL-6 antagonists** (e.g., tocilizumab, sarilumab) target the **interleukin-6 receptor**, reducing inflammatory responses driven by IL-6. - These drugs are used in conditions like **rheumatoid arthritis** and **giant cell arteritis**. *IL-10 antagonist* - **IL-10** is generally considered an **anti-inflammatory cytokine** that suppresses immune responses. - Antagonizing IL-10 would likely *promote* inflammation, and there are no widely used clinical drugs that function specifically as IL-10 antagonists.

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