General Pharmacology — MCQs

General Pharmacology Indian Medical PG Practice Questions and MCQs

Question 511: Hypomagnesemia due to increased excretion by the kidney is caused by all except:

A. Aminoglycoside
B. Furosemide
C. Cisplatin
D. Digitalis (Correct Answer)

Explanation: ***Digitalis*** - **Digitalis** (digoxin) is a cardiac glycoside that inhibits the **Na+/K+-ATPase pump**; it is not directly associated with renal magnesium wasting. Instead, its toxicity can be exacerbated by hypomagnesemia, but it does not cause it. - While it affects electrolyte balance intracellularly, it does not primarily lead to increased **urinary excretion of magnesium**. *Aminoglycoside* - **Aminoglycosides** like gentamicin can cause **renal tubular damage**, particularly in the distal tubules. - This damage impairs the kidney's ability to reabsorb magnesium, leading to increased **urinary magnesium excretion** and hypomagnesemia. *Furosemide* - **Furosemide** is a **loop diuretic** that inhibits the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle. - This inhibition reduces the **transepithelial potential difference**, which in turn reduces the passive reabsorption of magnesium and calcium, leading to increased urinary excretion. *Cisplatin* - **Cisplatin** is a chemotherapeutic agent known to cause **renal tubular toxicity**, particularly affecting the distal convoluted tubule. - This toxicity often results in impaired magnesium reabsorption and consequently increased **urinary magnesium loss**.

Question 512: Which drug does not cause rhinitis?

A. ACE inhibitors
B. Glucocorticoid (Correct Answer)
C. Reserpine
D. Prazosin

Explanation: ***Glucocorticoid*** - **Glucocorticoids** are the **first-line treatment** for allergic rhinitis, not a cause of rhinitis. - They work by reducing **inflammation** and **immune responses** in the nasal mucosa [1], [2]. - Intranasal corticosteroids effectively **prevent and treat** rhinitis symptoms [1]. *ACE inhibitors* - **ACE inhibitors** primarily cause a persistent, **dry cough** (10-20% of patients) due to accumulation of **bradykinin**. - Nasal congestion is **not a typical side effect**, though the bradykinin-mediated effects primarily manifest as cough rather than rhinitis. - The hallmark adverse effect is **cough**, not rhinitis. *Reserpine* - **Reserpine** causes **nasal congestion** and rhinitis as a well-documented side effect. - Mechanism: depletion of **norepinephrine** and catecholamines leads to increased **parasympathetic tone**. - This results in **vasodilation** and increased secretions in the nasal passages. *Prazosin* - **Prazosin**, an **alpha-1 adrenergic blocker**, commonly causes **nasal congestion** and rhinitis. - Mechanism: blocking alpha-1 receptors in nasal vasculature causes **vasodilation** and increased blood flow to the nasal mucosa. - This side effect is seen with all **alpha-blockers** and is well-documented.

Question 513: Drug commonly used as immunosuppressive therapy for non-infectious uveitis is -

A. Methotrexate
B. Infliximab
C. Voclosporin
D. Cyclosporine (Correct Answer)

Explanation: ***Cyclosporine*** - **Cyclosporine** is a **calcineurin inhibitor** that is commonly used as an immunosuppressive agent for **non-infectious uveitis**, particularly for sight-threatening or refractory cases [3]. - It works by inhibiting T-lymphocyte activation, thereby reducing intraocular inflammation [3]. - While effective, its use may be limited by side effects including **nephrotoxicity, hypertension, and hirsutism**. *Methotrexate* - **Methotrexate** is also **commonly used** as a first-line systemic immunosuppressive agent for non-infectious uveitis [1]. - It is an **antimetabolite** that inhibits dihydrofolate reductase, reducing inflammation and cell proliferation. - Often preferred due to its **favorable side effect profile** compared to cyclosporine, though both drugs are considered standard options. *Infliximab* - **Infliximab** is a **TNF-alpha inhibitor** (biologic agent) used for **severe or treatment-resistant uveitis**, particularly in cases associated with systemic inflammatory diseases like **Behçet's disease or ankylosing spondylitis** [2]. - It is generally considered a **second-line or third-line agent** after conventional immunosuppressants have failed. *Voclosporin* - **Voclosporin** is a **next-generation calcineurin inhibitor** primarily approved for **lupus nephritis**. - It is **not a standard therapy** for non-infectious uveitis and has limited data in this indication.

Question 514: All of the following statements are TRUE about second generation antihistaminic agents EXCEPT:

A. These may possess additional antiallergic mechanisms
B. These do not impair psychomotor performance
C. These lack anticholinergic actions
D. These possess high anti-motion sickness activity (Correct Answer)

Explanation: ***These possess high anti-motion sickness activity*** - Second-generation antihistamines have **poor penetration** into the central nervous system (CNS), making them ineffective for treating **motion sickness**. - **First-generation antihistamines**, which readily cross the blood-brain barrier and have **anticholinergic activity**, are typically used for motion sickness. *These may possess additional antiallergic mechanisms* - Many second-generation antihistamines, such as **cetirizine** and **loratadine**, have additional anti-inflammatory and **antiallergic properties** beyond H1 receptor blockade. - These mechanisms can include inhibiting the release of inflammatory mediators and **stabilizing mast cells**. *These do not impair psychomotor performance* - Second-generation antihistamines are **non-sedating** because they have limited ability to cross the **blood-brain barrier** and thus do not significantly affect CNS function. - This characteristic makes them suitable for use without causing **drowsiness** or impairing activities like driving. *These lack anticholinergic actions* - Unlike first-generation antihistamines, second-generation agents have **minimal to no affinity** for muscarinic acetylcholine receptors. - This lack of **anticholinergic activity** means they do not cause side effects such as **dry mouth**, blurred vision, or urinary retention.

Question 515: Which fully humanized antibody is used in treatment of rheumatoid arthritis?

A. Anakinra
B. Infliximab
C. Leflunomide
D. Adalimumab (Correct Answer)

Explanation: ***Adalimumab*** - **Adalimumab** is a **fully human monoclonal antibody** that targets **tumor necrosis factor-alpha (TNF-α)**, making it suitable for treating autoimmune conditions like rheumatoid arthritis without causing significant immunogenic reactions. - Its humanized structure minimizes the risk of developing **anti-drug antibodies**, improving long-term efficacy and safety. *Anakinra* - **Anakinra** is a **recombinant human interleukin-1 (IL-1) receptor antagonist**, not a fully humanized antibody. - While used in rheumatoid arthritis, its mechanism of action and structural classification differ from a fully humanized antibody. *Infliximab* - **Infliximab** is a **chimeric monoclonal antibody** (mouse-human), meaning it contains both mouse and human protein components. - It targets **TNF-α** but is not fully humanized, increasing the potential for immunogenicity compared to fully human antibodies. *Leflunomide* - **Leflunomide** is a **pyrimidine synthesis inhibitor**, functioning as an immunosuppressant rather than an antibody. - It works by inhibiting dihydroorotate dehydrogenase, which reduces lymphoid proliferation, making it a **disease-modifying antirheumatic drug (DMARD)**, not a biologic agent.

Question 516: Which of the following components is specifically used to enhance the antigenicity of a vaccine?

A. Preservative
B. Stabilizer
C. Adjuvant (Correct Answer)
D. None of the options

Explanation: ***Adjuvant*** - An **adjuvant** is a substance added to a vaccine to enhance the **immune response** to the antigen without having any specific antigenic properties itself. - They work by various mechanisms, such as forming a **depot** for the antigen, stimulating antigen-presenting cells, or activating innate immune pathways. *Preservative* - A **preservative** is included in some vaccines to prevent **microbial growth** and contamination, especially in multi-dose vials. - It does not enhance the immune response to the antigen. *Stabilizer* - A **stabilizer** helps maintain the **integrity** and **potency** of the vaccine's active ingredients over time and under varying storage conditions. - It prevents degradation of the antigen but does not directly boost its immunogenicity. *None of the options* - This option is incorrect because **adjuvants** are specifically designed and used to enhance the antigenicity of a vaccine. - The other listed components serve different purposes within a vaccine formulation.

Question 517: True regarding Conivaptan is -

A. Vasopressin Antagonist (Correct Answer)
B. Selective action on V2 receptors
C. Administered orally
D. Indicated for hypernatremia treatment

Explanation: ***Vasopressin Antagonist*** - **Conivaptan** is a non-peptide, dual **V1A and V2 vasopressin receptor antagonist**, blocking the actions of endogenous vasopressin [2], [3]. - By blocking these receptors, it promotes **aquaresis** (excretion of water without significant electrolyte loss), primarily used in cases of **hyponatremia** [1]. *Selective action on V2 receptors* - Conivaptan is a **dual antagonist**, acting on both **V1A and V2 receptors**, not selectively on V2 [2]. **Tolvaptan** is a selective V2 antagonist [1], [2]. - V2 selective antagonists are generally preferred for less off-target effects, but **conivaptan's dual action** can be useful in certain settings. *Administered orally* - Conivaptan is administered **intravenously**, it is **not available as an oral formulation** [3]. - **Tolvaptan**, another vasopressin antagonist, is available for **oral administration**. *Indicated for hypernatremia treatment* - Conivaptan is indicated for the treatment of **euvolemic and hypervolemic hyponatremia**, not hypernatremia [3]. - In hyponatremia, there is an excess of water relative to sodium, and conivaptan helps to **excrete this excess water**.

Question 518: What is the active ingredient of the marking nut (Semecarpus anacardium)?

A. Ricin
B. Croton
C. Semecarpol (Correct Answer)
D. Abrin

Explanation: ***Semecarpol*** - **Semecarpol** is a **phenolic compound** derived from the fruit of the marking nut tree (*Semecarpus anacardium*), which is responsible for its toxic and medicinal properties. - It causes **irritation**, **blistering**, and **allergic contact dermatitis** upon contact with skin. *Ricin* - **Ricin** is a **toxic protein** found in castor beans (*Ricinus communis*), not the marking nut. - It is a **potent ribosome-inactivating protein** that can be lethal if ingested, inhaled, or injected. *Croton* - **Croton** refers to a genus of plants (*Croton*) from which various compounds, including **phorbol esters**, can be extracted. - These compounds are potent **tumor promoters** and vesicants, but they are not the active ingredient of the marking nut. *Abrin* - **Abrin** is a **highly toxic protein** found in the seeds of the jequirity bean (*Abrus precatorius*), which is distinct from the marking nut. - Like ricin, abrin is a **ribosome-inactivating protein** and is extremely toxic upon exposure.

Question 519: Agent that acts through tyrosine kinase receptor is

A. Insulin (Correct Answer)
B. MSH
C. TSH
D. TRH

Explanation: ***Insulin*** - **Insulin** binds to its receptor, which is a **tyrosine kinase receptor**, leading to autophosphorylation and the activation of intracellular signaling pathways. - This activation is crucial for glucose uptake and metabolism by various cells in the body. *MSH* - **Melanocyte-stimulating hormone (MSH)** acts primarily through **G protein-coupled receptors**, specifically melanocortin receptors. - These receptors activate adenylyl cyclase, leading to an increase in intracellular cAMP. *TSH* - **Thyroid-stimulating hormone (TSH)** also acts via a **G protein-coupled receptor** on thyroid follicular cells. - Its binding stimulates adenylyl cyclase, increasing cAMP and thus thyroid hormone synthesis and release. *TRH* - **Thyrotropin-releasing hormone (TRH)** binds to **G protein-coupled receptors** on pituitary thyrotrophs. - This interaction activates the phospholipase C pathway, leading to the release of TSH.

Question 520: Reason for preferring Cisatracurium over Atracurium is:-

A. Faster acting than Atracurium
B. Shorter action than Atracurium
C. Lesser provocation of histamine release (Correct Answer)
D. Does not undergo Hoffman elimination

Explanation: ***Lesser provocation of histamine release*** - **Cisatracurium** is preferred over atracurium primarily due to its significantly **lower potential to induce histamine release**, leading to fewer cardiovascular side effects like hypotension and tachycardia. - This property makes cisatracurium a **safer option** for patients prone to hemodynamic instability or allergic reactions. *Faster acting than Atracurium* - Both atracurium and cisatracurium are **intermediate-acting** neuromuscular blockers, and their onset times are quite similar, with cisatracurium sometimes having a slightly *slower* onset. - The difference in onset time is **not clinically significant** enough to be a primary reason for preference. *Shorter action than Atracurium* - **Cisatracurium** has a slightly **longer duration of action** compared to atracurium, although both are considered intermediate-acting drugs. - Therefore, a shorter duration of action is **not a reason for its preference**; instead, it might even be a slight disadvantage in certain clinical scenarios requiring rapid reversal. *Does not undergo Hoffman elimination* - Both atracurium and cisatracurium undergo **Hoffman elimination** (non-enzymatic degradation) and ester hydrolysis, which allows for their use in patients with renal or hepatic dysfunction. - This is a shared characteristic, not a distinguishing factor that makes cisatracurium superior, and cisatracurium actually relies *more* heavily on Hoffman elimination.

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