General Pharmacology — MCQs

General Pharmacology Indian Medical PG Practice Questions and MCQs

Question 491: FK-506 is a

A. Opioid analgesic
B. Calcineurin inhibitor (Correct Answer)
C. Immunoglobulin antibody
D. Non depolarising muscle relaxant

Explanation: ***Calcineurin inhibitor*** - FK-506, also known as **tacrolimus**, is a potent **immunosuppressant** that inhibits the activity of calcineurin. - By inhibiting **calcineurin**, it prevents the dephosphorylation of **NFAT (Nuclear Factor of Activated T cells)**, thereby suppressing T-cell activation and proliferation. *Opioid analgesic* - **Opioid analgesics** are medications that relieve pain by binding to **opioid receptors** in the central nervous system. - Examples include morphine and fentanyl, which have a different mechanism of action and clinical use compared to FK-506. *Immunoglobulin antibody* - **Immunoglobulin antibodies** are proteins produced by plasma cells that target specific antigens to neutralize pathogens or toxins. - While therapeutic antibodies exist (e.g., monoclonal antibodies), FK-506 is a **small molecule drug** with a distinct mechanism of action, not an antibody. *Non depolarising muscle relaxant* - **Non-depolarizing muscle relaxants** are drugs that block the acetylcholine receptor at the neuromuscular junction, leading to muscle paralysis. - Examples include rocuronium and atracurium, which are used in anesthesia to facilitate intubation and ventilation, and are distinct from immunosuppressants.

Question 492: Number of doses of HDCV vaccine required for preexposure prophylaxis?

A. 3 (Correct Answer)
B. 5
C. 1
D. 7

Explanation: ***Correct Option: 3*** - Pre-exposure prophylaxis (PrEP) with **HDCV** (Human Diploid Cell Vaccine) typically involves a **three-dose series** administered on days 0, 7, and 21 or 28 for individuals at continuous or frequent risk of rabies exposure. - This schedule aims to establish immunity before potential exposure, providing a protective antibody response. *Incorrect Option: 5* - A five-dose regimen is typically reserved for **post-exposure prophylaxis (PEP)** in unvaccinated individuals after a rabies exposure. - This intensive schedule is designed to rapidly induce immunity when exposure is confirmed or highly suspected. *Incorrect Option: 1* - A single dose of HDCV is insufficient for establishing protective immunity against rabies, whether for pre-exposure or post-exposure prophylaxis. - A multi-dose series is required to prime the immune system and induce an adequate antibody response. *Incorrect Option: 7* - A seven-dose regimen is not a standard or recommended vaccination schedule for either pre-exposure or post-exposure prophylaxis against rabies. - Such an extended schedule would be medically unnecessary and deviate from established guidelines.

Question 493: Enuresis persists, and the patient is placed on desmopressin acetate (DDAVP). This medication works by which of the following mechanisms?

A. Decrease detrusor muscle tone
B. Increase water permeability and reabsorption in collecting tubules (Correct Answer)
C. Increase external sphincter contraction
D. Improves alertness of the patient during the sleep cycle

Explanation: ***Increase water permeability and reabsorption in collecting tubules*** - **Desmopressin acetate (DDAVP)** is a synthetic analog of **antidiuretic hormone (ADH)**, which acts on the V2 receptors in the **collecting tubules** of the kidneys [2], [3]. - This action increases the **permeability** of the collecting tubule cells to water, leading to increased **water reabsorption** and a reduction in urine production, thus controlling enuresis [1], [2]. *Decrease detrusor muscle tone* - This mechanism is associated with medications like **anticholinergics** (e.g., oxybutynin), which relax the **detrusor muscle** to reduce bladder contractions and urgency. - DDAVP does not directly affect the tone of the detrusor muscle; its primary action is on renal water handling [2]. *Increase external sphincter contraction* - Medications that strengthen the **external urethral sphincter** (e.g., alpha-adrenergic agonists) are used to improve continence in cases of stress incontinence. - DDAVP's mechanism is not related to sphincter contraction but rather to reducing the volume of urine produced [2]. *Improves alertness of the patient during the sleep cycle* - This mechanism would involve stimulating the central nervous system to awaken the patient when their bladder is full. - DDAVP does not act as a central nervous system stimulant and does not affect the patient's sleep cycle or alertness [2].

Question 494: Tolvaptan is a/an -

A. ACE inhibitor
B. Renin inhibitor
C. Vasopressin antagonist (Correct Answer)
D. Angiotensin antagonist

Explanation: ***Vasopressin antagonist*** - **Tolvaptan** specifically blocks the action of **vasopressin (antidiuretic hormone)** at the V2 receptor. - This action leads to increased water excretion without affecting electrolyte balance, making it useful in treating conditions like **hyponatremia** and **syndrome of inappropriate antidiuretic hormone secretion (SIADH)**. *ACE inhibitor* - **ACE inhibitors** like captopril or enalapril block the conversion of **angiotensin I to angiotensin II**, reducing vasoconstriction and aldosterone release. - They are primarily used for **hypertension**, **heart failure**, and **diabetic nephropathy**, which is a different mechanism of action than tolvaptan. *Renin inhibitor* - **Renin inhibitors**, such as aliskiren, directly block the **renin enzyme**, preventing the formation of angiotensin I. - This mechanism also targets the **renin-angiotensin-aldosterone system (RAAS)** but at an earlier step than an ACE inhibitor. *Angiotensin antagonist* - **Angiotensin receptor blockers (ARBs)**, such as losartan or valsartan, block the binding of **angiotensin II** to its AT1 receptor. - Similar to ACE inhibitors, they are used for **hypertension** and **heart failure** but do not directly affect vasopressin.

Question 495: Acetazolamide is associated with:

A. Metabolic acidosis (Correct Answer)
B. Both metabolic acidosis and alkalosis
C. Metabolic alkalosis
D. None of the above

Explanation: ***Metabolic acidosis*** - **Acetazolamide** inhibits **carbonic anhydrase** in the proximal renal tubules, reducing H+ secretion and **bicarbonate reabsorption**. - This leads to increased urinary excretion of bicarbonate (HCO3-), resulting in **hyperchloremic normal anion gap metabolic acidosis**. - Clinically used in conditions like glaucoma, altitude sickness, and metabolic alkalosis correction. *Both metabolic acidosis and alkalosis* - While acetazolamide causes **metabolic acidosis**, it does not cause **metabolic alkalosis**. - The mechanism of action specifically inhibits bicarbonate reabsorption, leading only to acidosis, not alkalosis. *Metabolic alkalosis* - **Metabolic alkalosis** is characterized by an excess of bicarbonate, which is the opposite effect of acetazolamide. - Medications that can cause metabolic alkalosis include loop diuretics (through volume contraction) or thiazide diuretics, not carbonic anhydrase inhibitors. *None of the above* - This option is incorrect because **acetazolamide** is definitively associated with **metabolic acidosis**. - The drug's mechanism of action directly leads to this characteristic acid-base disturbance.

Question 496: In osteoporosis, bone formation is increased by which drug?

A. Estrogen
B. Bisphosphonates
C. Teriparatide (Correct Answer)
D. Calcitonin

Explanation: ***Teriparatide*** - Teriparatide is a recombinant form of **parathyroid hormone (PTH)** that, when administered intermittently, stimulates **osteoblast activity** leading to increased **bone formation**. - It is an **anabolic agent** used in osteoporosis to build new bone rather than just prevent bone loss. *Estrogen* - Estrogen is primarily used to prevent **bone loss** by **inhibiting osteoclast activity** and supporting bone mineralization. - It does not directly **increase bone formation** but rather maintains bone density. *Bisphosphonates* - Bisphosphonates inhibit **osteoclast-mediated bone resorption** by inducing apoptosis in osteoclasts. - They primarily **decrease bone breakdown** and do not directly stimulate new bone formation. *Calcitonin* - Calcitonin is a hormone that **inhibits osteoclast activity** and thus reduces bone resorption. - It is not a bone-forming agent but rather acts to **decrease bone breakdown** and is used for pain relief in vertebral fractures.

Question 497: Botulinum toxin is used in -

A. Myasthenia gravis
B. Cerebellar ataxia
C. Focal dystonia (Correct Answer)
D. Hypotonia

Explanation: ***Focal dystonia*** - **Botulinum toxin** is a potent neurotoxin that relaxes muscles by blocking the release of **acetylcholine** at the neuromuscular junction. - In **focal dystonia**, specific muscles contract involuntarily, causing abnormal postures or movements; botulinum toxin injections can temporarily paralyze these muscles, reducing symptoms. *Myasthenia gravis* - **Myasthenia gravis** is an **autoimmune disease** characterized by muscle weakness due to antibodies blocking **acetylcholine receptors** at the neuromuscular junction. - Injecting **botulinum toxin** would further weaken the already compromised muscles, exacerbating the condition, and is therefore contraindicated. *Cerebellar ataxia* - **Cerebellar ataxia** results from damage to the **cerebellum**, leading to problems with coordination, balance, and fine motor control. - **Botulinum toxin** acts on the neuromuscular junction and would not address the underlying neurological deficit in the cerebellum. *Hypotonia* - **Hypotonia** refers to decreased muscle tone, often caused by problems in the brain, spinal cord, nerves, or muscles. - Using **botulinum toxin**, which causes muscle paralysis, would worsen **hypotonia** by further reducing muscle tone and strength.

Question 498: The following smooth muscle relaxants act by affecting calcium release except:

A. Dantrolene
B. Nifedipine
C. Prazosin (Correct Answer)
D. Verapamil

Explanation: ***Prazosin*** - Prazosin is an **alpha-1 adrenergic receptor antagonist** that causes smooth muscle relaxation by blocking the vasoconstrictive effects of norepinephrine, **not by directly affecting calcium release or calcium channels** [4]. - Its mechanism involves preventing receptor-mediated vasoconstriction through downstream signaling pathways, which are distinct from direct calcium channel modulation or calcium release from intracellular stores. - **This is the correct answer** as it does not act by affecting calcium handling. *Dantrolene* - Dantrolene acts by inhibiting the release of **calcium from the sarcoplasmic reticulum** in muscle cells by blocking **ryanodine receptors (RyR1)**. - **Important note:** Dantrolene is primarily a **skeletal muscle relaxant** used for malignant hyperthermia and spasticity, not a typical smooth muscle relaxant. - While it does affect calcium release, its primary therapeutic action is on skeletal muscle, making its inclusion in "smooth muscle relaxants" questionable. *Nifedipine* - Nifedipine is a **dihydropyridine calcium channel blocker** that inhibits the influx of extracellular calcium into smooth muscle cells [2]. - By blocking **L-type voltage-gated calcium channels**, it reduces intracellular calcium availability, leading to smooth muscle relaxation, particularly in vascular smooth muscle [1], [3]. *Verapamil* - Verapamil is a **non-dihydropyridine calcium channel blocker** that also inhibits the influx of extracellular calcium into smooth muscle cells [3]. - It primarily affects **L-type calcium channels** in both cardiac and smooth muscle, leading to vasodilation and reduced cardiac contractility [1], [2].

Question 499: Allopurinol is used in organ preservation as:

A. Precursor for energy metabolism
B. Preservative
C. Antioxidant (Correct Answer)
D. Free radical scavenger

Explanation: ***Antioxidant*** - Allopurinol acts as a **xanthine oxidase inhibitor**, which reduces the production of **superoxide radicals** during reperfusion injury. - By inhibiting this enzyme, it indirectly limits the formation of harmful **reactive oxygen species**, thereby functioning as an effective antioxidant in organ preservation. *Precursor for energy metabolism* - Allopurinol is an **inhibitor of purine metabolism**, specifically xanthine oxidase, rather than a precursor. - Its metabolic action works against energy production in the context of purine synthesis. *Preservative* - While it aids in organ preservation due to its pharmacological effects, "preservative" is a general term and doesn't specify its mechanism of action. - Its role is targeted at specific biochemical pathways, not broadly as a non-specific preserving agent. *Free radical scavenger* - While allopurinol does reduce free radicals, it does so indirectly by **inhibiting their production**, rather than through direct scavenging. - It prevents the formation of **superoxide anions** by blocking the enzyme responsible for their synthesis, rather than chemically neutralizing existing ones.

Question 500: Atropine is the drug of choice in –

A. Chorioretinitis
B. Lens induced glaucoma
C. Iridocyclitis (Correct Answer)
D. Closed angle glaucoma

Explanation: ***Iridocyclitis*** - Atropine is a **potent cycloplegic and mydriatic agent** often used in iridocyclitis to **relax the ciliary body muscles** and prevent the formation of posterior synechiae. - Its **long-acting effect** helps in reducing pain, inflammation, and preventing complications such as iris bombe by keeping the pupil dilated. *Chorioretinitis* - This condition primarily affects the **choroid and retina**, and while inflammation may be present, systemic or topical **corticosteroids** are typically the primary treatment. - Atropine is not indicated as a primary treatment for the inflammation itself in chorioretinitis, as its main action is on the iris and ciliary body. *Lens induced glaucoma* - The definitive treatment for lens-induced glaucoma, such as **phacomorphic glaucoma** or **phacolytic glaucoma**, is surgical removal of the cataractous lens. - Atropine would cause mydriasis, which can paradoxically worsen some forms of glaucoma by blocking the drainage angle, especially in cases of angle closure [1] [2]. *Closed angle glaucoma* - Atropine, being a mydriatic, would **dilate the pupil** and potentially exacerbate closed-angle glaucoma by further **crowding the anterior chamber angle** and blocking aqueous humor outflow [3]. - The focus in closed-angle glaucoma is to constrict the pupil (with miotics like pilocarpine) and reduce intraocular pressure.

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