General Pharmacology — MCQs

General Pharmacology Indian Medical PG Practice Questions and MCQs

Question 471: Mechanism of action of allopurinol is

A. Recombinant uricase
B. Decrease chemotaxis
C. Increase uric acid excretion
D. Xanthine oxidase inhibition (Correct Answer)

Explanation: ***Xanthine oxidase inhibition*** - **Allopurinol** acts as a **structural analog of hypoxanthine** and competitively inhibits the enzyme **xanthine oxidase**. - By inhibiting **xanthine oxidase**, allopurinol prevents the conversion of hypoxanthine to xanthine and then to uric acid, thereby **decreasing uric acid production**. *Recombinant uricase* - **Recombinant uricase** (e.g., rasburicase, pegloticase) is an enzyme that catalyzes the breakdown of existing uric acid into allantoin, a more soluble compound. - This mechanism is distinct from allopurinol, which **prevents uric acid formation**. *Decrease chemotaxis* - Medications that **decrease chemotaxis**, such as **colchicine**, work by interfering with the migration of neutrophils to sites of inflammation, which is useful in acute gout flares. - This is an **anti-inflammatory mechanism**, not related to uric acid synthesis or excretion. *Increase uric acid excretion* - Drugs that **increase uric acid excretion** are known as **uricosurics** (e.g., probenecid, lesinurad). - These agents act on the renal tubules to **inhibit uric acid reabsorption**, thus promoting its elimination from the body.

Question 472: What is the dose of mifepristone in emergency contraception?

A. 25 mg
B. 200 mcg
C. 200 mg
D. 10 mg (Correct Answer)

Explanation: ***10 mg*** - **10 mg is the WHO-recommended dose** of mifepristone for emergency contraception. - This single dose is **equally effective** as higher doses (25-50 mg) and works primarily by **delaying or inhibiting ovulation**. - It has been validated through **multiple international clinical trials** and is the standard regimen used globally. - When taken within **72-120 hours** of unprotected intercourse, it significantly reduces pregnancy risk. *25 mg* - While 25 mg of mifepristone has been studied for emergency contraception and shows efficacy, it is **not the standard recommended dose**. - The **10 mg dose is preferred** as it achieves similar efficacy with potentially fewer side effects and lower cost. - Some countries may use 25 mg, but **WHO guidelines recommend 10 mg** as the optimal dose. *200 mg* - A 200 mg dose of mifepristone is typically utilized for **medical abortion regimens**, often in combination with a prostaglandin analog (misoprostol). - This dosage achieves a different pharmacological effect, leading to **detachment of the embryo** and uterine contractions. - This is **far higher than needed** for emergency contraception purposes. *200 mcg* - **Mifepristone is not dosed in micrograms** (mcg) for emergency contraception or medical abortion; it is measured in milligrams (mg). - This unit and dosage are more commonly associated with other medications, such as **misoprostol** when used for obstetric indications. - 200 mcg would be 0.2 mg, which is **subtherapeutic** for any mifepristone indication.

Question 473: Which of the following is the shortest-acting corticosteroid?

A. Dexamethasone
B. Hydrocortisone (Correct Answer)
C. Triamcinolone
D. Deflazacort

Explanation: ***Hydrocortisone***- **Hydrocortisone** is considered a **short-acting corticosteroid** with a biological half-life of 8-12 hours [1].- It is a naturally occurring glucocorticoid, acting as a direct replacement for cortisol.- Among the given options, it has the shortest duration of action.*Dexamethasone*- **Dexamethasone** is a **long-acting corticosteroid** with a biological half-life of 36-72 hours.- Its potent and prolonged action makes it suitable for conditions requiring sustained anti-inflammatory or immunosuppressive effects.*Triamcinolone*- **Triamcinolone** is an **intermediate-acting corticosteroid** with a biological half-life typically ranging from 18-36 hours.- It is commonly used for its anti-inflammatory effects in conditions like allergies, asthma, and skin disorders.*Deflazacort*- **Deflazacort** is an **intermediate-acting corticosteroid** with a duration of action of approximately 12-18 hours.- It is a prodrug that is metabolized to 21-desacetyl deflazacort, the active form, often used in conditions like Duchenne muscular dystrophy and inflammatory disorders.

Question 474: Allopurinol inhibits which enzyme?

A. Lysyl oxidase
B. Xanthine oxidase (Correct Answer)
C. Cyclooxygenase
D. Kinase

Explanation: ***Xanthine oxidase*** - Allopurinol is a **purine analog** that acts as a **competitive inhibitor** of the enzyme **xanthine oxidase**. - By inhibiting xanthine oxidase, allopurinol prevents the conversion of **hypoxanthine to xanthine** and subsequently to **uric acid**, thereby lowering serum uric acid levels. *Lysyl oxidase* - **Lysyl oxidase** is an enzyme involved in the **cross-linking of collagen and elastin**, crucial for the stability of connective tissues. - Its inhibition would not directly affect **uric acid metabolism** or be a mechanism of allopurinol's action. *Cyclooxygenase* - **Cyclooxygenase (COX)** is a key enzyme in the synthesis of **prostaglandins and thromboxanes** from arachidonic acid, mediating inflammation and pain. - **NSAIDs** are inhibitors of cyclooxygenase, not allopurinol. *Kinase* - **Kinases** are a broad class of enzymes that **catalyze the transfer of phosphate groups** from high-energy molecules (like ATP) to specific substrates. - While essential for many cellular processes, kinases are not the specific target of **allopurinol** in uric acid reduction.

Question 475: Which of the following is a G protein coupled receptor?

A. M2 muscarinic receptor (Correct Answer)
B. NMDA receptor
C. Insulin receptors
D. Steroid receptors

Explanation: ***M2 muscarinic receptor***- The **M2 muscarinic receptor** is a classic example of a **G protein-coupled receptor (GPCR)** [1]. When a ligand binds to a G-protein-coupled receptor, it triggers a mechanism where GDP is exchanged for GTP, causing the G-protein's alpha subunit to separate and initiate signaling pathways [1]. These heterotrimeric G-proteins couple cell surface receptors to catalytic units that form second messengers or directly to ion channels [1]. GPCRs are important regulators of nerve activity in the CNS and are receptors for neurotransmitters of the peripheral autonomic nervous system, with acetylcholine (ACh) being a ligand that regulates functions of glands and smooth muscle [2]. The **M2 muscarinic receptor** specifically activates an **inhibitory G protein (G_i)**, leading to a decrease in **cAMP** and opening of **potassium channels**. The effects of metabotropic receptors, like GPCRs, can last tens of seconds to minutes, contrasting with the brief effects of ionotropic receptors [4].*NMDA receptor*- The **NMDA receptor** is a **ligand-gated ion channel** that allows the influx of calcium and sodium ions [3]. It does not couple to G proteins, but directly mediates ion flow upon activation by **glutamate** and **glycine**. Ligand-gated ion channels open a central transmembrane ion channel when a neurotransmitter binds to sites on its extracellular domain [3].*Steroid*- **Steroid hormones** primarily act on **intracellular receptors** that, once activated, translocate to the nucleus to regulate gene expression. They are not cell surface receptors and do not utilize G protein signaling.*Insulin receptors*- **Insulin receptors** are **receptor tyrosine kinases** that, upon binding insulin, undergo autophosphorylation and activate intracellular signaling pathways. They signal through a cascade of protein phosphorylations, not through G proteins.

Question 476: Retention of sodium is a side effect of:

A. Triamcinolone
B. Corticosterone
C. Prednisolone
D. Hydrocortisone (Correct Answer)

Explanation: ***Hydrocortisone*** - **Hydrocortisone** possesses some **mineralocorticoid activity**, particularly at higher doses, leading to **sodium retention** and potassium excretion. - This mineralocorticoid effect can cause side effects like **edema** and **hypertension** due to increased fluid volume. *Triamcinolone* - **Triamcinolone** is a synthetic corticosteroid with **negligible mineralocorticoid activity**. - It is often favored when **sodium retention** is undesirable, as it primarily exerts **glucocorticoid effects**. *Corticosterone* - **Corticosterone** is a natural glucocorticoid with less potent **mineralocorticoid activity** than aldosterone but more than most synthetic glucocorticoids. - While it can cause some **sodium retention**, it is not a commonly prescribed medication and its effect is less pronounced than **hydrocortisone** at equipotent doses in clinical settings. *Prednisolone* - **Prednisolone** has minimal **mineralocorticoid activity** compared to hydrocortisone. - It is primarily a **glucocorticoid** used for its anti-inflammatory and immunosuppressive effects with a lower risk of **sodium retention**.

Question 477: Which fluoride compound is most effective for bacterial enzyme inhibition after topical application:

A. NaF
B. APF
C. Sodium mono-fluorophosphate
D. SnF2 (Correct Answer)

Explanation: ***Correct: SnF2 (Stannous Fluoride)*** - **Stannous fluoride (SnF2)** is the most effective fluoride compound for **bacterial enzyme inhibition** after topical application - Provides **dual antimicrobial mechanism**: fluoride ions inhibit enolase in glycolysis, while stannous ions (Sn²⁺) have **direct bactericidal effects** and inhibit multiple bacterial enzymes - The **stannous ion** penetrates bacterial cell walls and disrupts enzyme systems more effectively than fluoride alone - Superior at inhibiting **acid production** by cariogenic bacteria through enhanced enzyme interference - Clinically proven **anti-plaque** and **antimicrobial** properties beyond simple fluoride action *Incorrect: NaF (Sodium Fluoride)* - While NaF releases fluoride ions that inhibit bacterial enolase, it lacks the additional antimicrobial activity of the stannous ion - Its primary mechanism is **remineralization** of enamel through fluorapatite formation, not superior bacterial enzyme inhibition - Less effective than SnF2 for direct antibacterial enzyme inhibition *Incorrect: Sodium mono-fluorophosphate* - Requires **enzymatic hydrolysis** by bacterial or salivary phosphatases to release free fluoride ions - This delayed release makes it **less effective** for immediate bacterial enzyme inhibition - Preferred in toothpastes for chemical stability, not for antimicrobial efficacy *Incorrect: APF (Acidulated Phosphate Fluoride)* - Low pH enhances **fluoride uptake into enamel** for remineralization - Primary advantage is **fluorapatite formation** and enamel strengthening - Not specifically superior for bacterial enzyme inhibition compared to SnF2's dual-action mechanism

Question 478: Which of the following is false about drugs given in urinary incontinence

A. Oxybutynin, Tolterodine, and Solifenacin are muscarinic receptor blockers used to decrease detrusor muscle contraction
B. Tolterodine can be given as transdermal patch (Correct Answer)
C. Darifenacin is a selective M3 antagonist
D. Trospium is a quaternary amine with no CNS side effects

Explanation: ***Tolterodine can be given as transdermal patch*** - This statement is **false**. While tolterodine is available in oral forms, such as extended-release capsules, it is **not available as a transdermal patch**. - **Oxybutynin** is the muscarinic antagonist commonly available and administered as a transdermal patch for urinary incontinence. *Oxybutynin, Tolterodine, and Solifenacin are muscarinic receptor blockers used to decrease detrusor muscle contraction* - This statement is **true**; these drugs are indeed anticholinergics that block muscarinic receptors (primarily M3) on the detrusor muscle. - By blocking these receptors, they reduce the involuntary contractions of the detrusor, thereby alleviating symptoms of **overactive bladder** and urgency incontinence. *Darifenacin is a selective M3 antagonist* - This statement is **true**; **darifenacin** is known for its high selectivity for the **M3 muscarinic receptor**. - This selectivity makes it effective in treating **overactive bladder** with potentially fewer side effects in other organ systems compared to less selective anticholinergics. *Trospium is a quaternary amine with no CNS side effects* - This statement is **true**; **trospium** is a **quaternary amine**, which means it has a permanent positive charge. - Due to its charge, it has **poor lipid solubility** and does not readily cross the **blood-brain barrier**, resulting in a significantly lower incidence of central nervous system (CNS) side effects compared to tertiary amines.

Question 479: Regarding BCG vaccine, which of the following is untrue?

A. T.B. vaccine
B. All of the options
C. live vaccine
D. Orally administered (Correct Answer)

Explanation: ***Orally administered*** - The **BCG vaccine** is not administered orally; it is typically given via an **intradermal injection**, usually in the upper arm. - Oral administration is a route used for some vaccines, but not for BCG. *T.B. vaccine* - The **BCG vaccine** is indeed a vaccine against **tuberculosis (TB)**, making this statement true. - It works by using a live, attenuated strain of *Mycobacterium bovis* to provide immunity against *Mycobacterium tuberculosis*. *All of the options* - Since the statement "Orally administered" is untrue, this option cannot be correct. - The BCG vaccine is not administered orally, which makes that specific claim false. *live vaccine* - The **BCG vaccine** is a **live attenuated vaccine**, meaning it contains a weakened form of the *Mycobacterium bovis* bacterium. - This characteristic allows it to stimulate a strong immune response, making this statement true.

Question 480: Which of the following increases uric acid excretion?

A. Probenecid (Correct Answer)
B. Allopurinol
C. Aspirin
D. Colchicine

Explanation: **Probenecid** - **Probenecid** is a **uricosuric agent** that increases renal excretion of uric acid by inhibiting its reabsorption in the proximal tubule. - It is used in the treatment of **chronic gout** to lower serum uric acid levels. *Allopurinol* - **Allopurinol** works by inhibiting **xanthine oxidase**, an enzyme responsible for uric acid synthesis, thereby reducing its production. - It does not increase uric acid excretion but rather decreases its formation, making it suitable for **overproducers** of uric acid. *Aspirin* - **Low-dose aspirin** can actually *decrease* uric acid excretion by interfering with tubular secretion of uric acid. - **High-dose aspirin** has a uricosuric effect, but it is not typically used for gout due to side effects and more effective alternatives. *Colchicine* - **Colchicine** is an **anti-inflammatory agent** used to treat acute gout flares by inhibiting neutrophil chemotaxis and activation. - It does **not affect uric acid synthesis or excretion** directly, but rather mitigates the inflammatory response to uric acid crystals.

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