General Pharmacology — MCQs

General Pharmacology Indian Medical PG Practice Questions and MCQs

Question 591: What is the mechanism of action of Abatacept?

A. Tumor necrosis factor (TNF) alpha inhibitor
B. Monoclonal antibody against interleukin-6 (IL-6) receptor
C. Interleukin-1 (IL-1) receptor antagonist
D. Inhibitor of co-stimulation of T cells (Correct Answer)

Explanation: ***Inhibitor of co-stimulation of T cells*** - Abatacept is a **fusion protein** that blocks the **CD28-CD80/86 co-stimulatory pathway**, which is crucial for full T-cell activation. - By binding to **CD80** and **CD86** on antigen-presenting cells, it prevents their interaction with **CD28** on T cells, thus inhibiting T-cell proliferation and cytokine production. *Tumor necrosis factor (TNF) alpha inhibitor* - TNF alpha inhibitors (e.g., **adalimumab**, **infliximab**, **etanercept**) bind to and neutralize **TNF alpha**, a pro-inflammatory cytokine. - While used in similar conditions, their mechanism is distinct from Abatacept's T-cell co-stimulation blockade. *Monoclonal antibody against interleukin-6 (IL-6) receptor* - Drugs like **tocilizumab** target the **IL-6 receptor**, blocking the signaling of **IL-6**, another important inflammatory cytokine. - This mechanism primarily affects cytokine signaling rather than directly inhibiting T-cell activation in the same way as abatacept. *Interleukin-1 (IL-1) receptor antagonist* - **Anakinra** is an example of an **IL-1 receptor antagonist**, which competes with IL-1 for binding to its receptor, thereby blocking its pro-inflammatory effects. - This mechanism focuses on inhibiting the action of IL-1, unlike Abatacept's role in T-cell activation.

Question 592: Beta2-agonists cause all except:

A. Hyperkalemia (Correct Answer)
B. Hyperglycemia
C. Tremor
D. Palpitation

Explanation: ***Hyperkalemia*** - Beta2-agonists actually cause **hypokalemia**, not hyperkalemia, by promoting the intracellular shift of potassium. - This effect is due to the stimulation of the **Na+/K+-ATPase pump** by beta-2 adrenergic receptors. *Hyperglycemia* - Beta2-agonists can lead to **hyperglycemia** by promoting glycogenolysis and gluconeogenesis in the liver. - They also decrease **insulin secretion** and increase insulin resistance. *Tremor* - **Tremor** is a common side effect of beta2-agonists, particularly in the hands, due to direct stimulation of beta2 receptors on skeletal muscle. - This muscle stimulation leads to increased muscle twitching and a fine tremor. *Palpitation* - **Palpitations** can occur due to the systemic absorption of beta2-agonists, leading to activation of beta1 receptors in the heart. - This can cause **tachycardia** and a sensation of a racing heart.

Question 593: Ranibizumab is a monoclonal antibody against?

A. VEGF (Correct Answer)
B. Interleukin-6
C. Cluster of Differentiation 20
D. Epidermal Growth Factor Receptor

Explanation: ***VEGF*** - **Ranibizumab** is a **monoclonal antibody** specifically designed to inhibit **vascular endothelial growth factor A (VEGF-A)**. - By binding to VEGF-A, ranibizumab prevents its interaction with receptors on endothelial cells, thereby inhibiting **angiogenesis** and reducing vascular permeability, which is crucial in treating conditions like **wet age-related macular degeneration (AMD)** and **diabetic macular edema**. *Interleukin-6* - **Interleukin-6 (IL-6)** is a **pro-inflammatory cytokine** involved in various autoimmune and inflammatory diseases. - Monoclonal antibodies targeting IL-6, such as **tocilizumab**, are used in conditions like **rheumatoid arthritis** and **cytokine release syndrome**, not for ocular neovascularization. *Cluster of Differentiation 20* - **Cluster of Differentiation 20 (CD20)** is a protein found on the surface of **B lymphocytes**. - Monoclonal antibodies against CD20, like **rituximab**, are used in the treatment of **B-cell lymphomas**, **leukemia**, and certain **autoimmune diseases**, not for conditions requiring anti-VEGF therapy. *Epidermal Growth Factor Receptor* - The **epidermal growth factor receptor (EGFR)** is a **tyrosine kinase receptor** involved in cell growth and proliferation. - Monoclonal antibodies targeting EGFR, such as **cetuximab** and **panitumumab**, are used in the treatment of various **cancers**, particularly **colorectal cancer** and **head and neck cancer**.

Question 594: Pyridoxine is used in treatment of ?

A. Galactosemia
B. Phenylketonuria
C. Propionic acidemia
D. Homocystinuria (Correct Answer)

Explanation: ***Homocystinuria*** - **Pyridoxine (vitamin B6)** is a cofactor for the enzyme **cystathionine beta-synthase**, which is deficient in many forms of homocystinuria. - In pyridoxine-responsive homocystinuria, high doses of pyridoxine can help reduce **homocysteine levels** by stimulating residual enzyme activity. *Galactosemia* - This is an inherited disorder affecting the body's ability to metabolize **galactose**, due to deficiency of enzymes like galactose-1-phosphate uridyltransferase. - Treatment primarily involves dietary restriction of **galactose** and lactose, not pyridoxine. *Phenylketonuria* - This metabolic disorder results from a deficiency in **phenylalanine hydroxylase**, leading to a buildup of phenylalanine. - Treatment involves a strict **low-phenylalanine diet** and sometimes sapropterin (BH4). *Propionic acidemia* - This organic acidemia is caused by a deficiency in **propionyl-CoA carboxylase**, an enzyme requiring **biotin** as a cofactor. - Treatment involves dietary protein restriction and often carnitine supplementation, with **biotin** sometimes used, but not pyridoxine.

Question 595: When two different chemicals act on two different receptors and their responses are opposite to each other on the same cell, this phenomenon is called?

A. Physiological antagonism (Correct Answer)
B. Chemical antagonism
C. Reversible antagonism
D. Competitive antagonism

Explanation: ***Physiological antagonism*** - This occurs when two drugs act on **different receptors** to produce **opposite physiological effects** within the same system or cell, effectively canceling each other out [1]. - A classic example is the opposing actions of **histamine** (causing bronchoconstriction) and **adrenaline** (causing bronchodilation) on the bronchi [1]. *Chemical antagonism* - This involves a direct **chemical interaction** between two drugs that results in the **inactivation of one or both** of them. - An example is the binding of **chelating agents** to heavy metals, forming an inert complex. *Reversible antagonism* - This describes antagonism where the antagonist binds to the receptor and can be **displaced by a higher concentration of the agonist**. - It does not specifically describe antagonists acting on different receptors or producing opposing physiological effects. *Competitive antagonism* - This occurs when an antagonist directly **competes with an agonist for the same binding site** on a receptor [1]. - The antagonist, while not producing a response itself, prevents the agonist from binding and activating the receptor.

Question 596: Which of the following is not an ionic receptor?

A. Kainate
B. AMPA
C. mGluR (Correct Answer)
D. NMDA

Explanation: **Ionic receptors** (ionotropic receptors) are ligand-gated ion channels that open upon binding, allowing ions to flow directly through the channel. **Non-ionic receptors** (metabotropic receptors) are G-protein coupled receptors that activate intracellular signaling cascades. ***mGluR*** - **Metabotropic glutamate receptors (mGluRs)** are **G-protein coupled receptors** (GPCRs), meaning they activate intracellular signaling pathways rather than directly forming an ion channel. - Their activation leads to slower, longer-lasting changes in neuronal excitability through second messenger systems. - **This is the correct answer** as mGluRs are NOT ionic receptors. *NMDA* - **NMDA receptors** are **ionotropic glutamate receptors** that form ligand-gated ion channels permeable to calcium and sodium ions. - They are crucial for **synaptic plasticity** and learning. *Kainate* - **Kainate receptors** are also **ionotropic glutamate receptors** that are permeable to sodium and potassium ions. - They play diverse roles in synaptic transmission and neuronal excitability. *AMPA* - **AMPA receptors** are **ionotropic glutamate receptors** primarily responsible for fast excitatory synaptic transmission in the central nervous system. - They are permeable to sodium and potassium ions and mediate the majority of fast excitatory synaptic currents.

Question 597: Which of the following act through G protein coupled receptors?

A. Ach Muscarinic receptors (Correct Answer)
B. Insulin receptors
C. Ach Nicotinic receptors
D. GABA-A receptors

Explanation: ***Ach Muscarinic receptors*** - All five **muscarinic acetylcholine receptors (M1-M5)** are **G protein-coupled receptors (GPCRs)** that mediate the parasympathetic nervous system's effects. - Activation of these receptors leads to downstream signaling through various G proteins, influencing cellular functions like heart rate and smooth muscle contraction. *Insulin receptors* - Insulin receptors are **receptor tyrosine kinases (RTKs)**, not GPCRs. - Upon insulin binding, they undergo autophosphorylation and activate intracellular signaling cascades involving **IRS proteins**, leading to glucose uptake. *Ach Nicotinic receptors* - Nicotinic acetylcholine receptors are **ligand-gated ion channels**, not GPCRs. - They open an ion pore in response to acetylcholine binding, allowing ions like sodium to flow through, resulting in rapid depolarization. *GABA-A receptors* - GABA-A receptors are also **ligand-gated ion channels**, specifically anion channels that are permeable to chloride ions. - When GABA binds, they open, allowing chloride influx, which typically hyperpolarizes the neuron and inhibits neural activity.

Question 598: Which of the following is not a definite use for Prostaglandin E2 (PGE2)?

A. Induces labour
B. Keeps patency of PDA (Correct Answer)
C. Contraception
D. Therapeutic abortion

Explanation: ***Keeps patency of PDA*** - **Prostaglandin E1 (PGE1)**, not PGE2, is used to maintain the patency of the **ductus arteriosus** in neonates with certain congenital heart defects. - PGE1 causes **vascular smooth muscle relaxation**, preventing closure of the ductus arteriosus. *Contraception* - **PGE2 analogs** are used in various forms of contraception, including emergency contraception and for cervical ripening before elective abortion. - They act by inducing **uterine contractions** and can interfere with implantation or facilitate expulsion of a fertilized egg. *Induces labour* - **PGE2 (dinoprostone)** is commonly used clinically to induce labor by promoting **cervical ripening** and stimulating **uterine contractions**. - It is administered as a vaginal gel or insert to prepare the cervix for delivery. *Therapeutic abortion* - **PGE2 analogs** are used to induce therapeutic abortion, particularly in the second trimester, by causing powerful **uterine contractions** that lead to the expulsion of the fetus. - They are often used in combination with other agents to enhance their efficacy.

Question 599: Which local anesthetic is known for its vasoconstrictive properties?

A. Lidocaine
B. Chlorprocaine
C. Procaine
D. Cocaine (Correct Answer)

Explanation: ***Cocaine*** - Cocaine is unique among local anesthetics for its inherent **sympathomimetic** properties, leading to **vasoconstriction**. - This vasoconstriction is due to its ability to block the reuptake of **norepinephrine** and other catecholamines at adrenergic nerve terminals. *Procaine* - Procaine is an **ester-type** local anesthetic that typically causes **vasodilation**, which can lead to rapid systemic absorption and a shorter duration of action. - It does not possess any inherent vasoconstrictive properties. *Lidocaine* - Lidocaine, an **amide-type** local anesthetic, generally causes **vasodilation** at clinical concentrations. - Due to this vasodilatory effect, **epinephrine** is often added to lidocaine preparations to prolong its action and reduce systemic absorption. *Chlorprocaine* - Chlorprocaine is another **ester-type** local anesthetic known for its rapid onset and short duration of action. - It primarily causes **vasodilation**, similar to procaine, and has no intrinsic vasoconstrictive effects.

Question 600: Midazolam does not cause which of the following?

A. Anterograde amnesia
B. Decreased cardiovascular effects as compared to propofol
C. Causes tachyphylaxis during high dose infusions
D. Retrograde amnesia (Correct Answer)

Explanation: ***Retrograde amnesia*** - Midazolam, a benzodiazepine, primarily causes **anterograde amnesia** [2], meaning patients have difficulty forming new memories after drug administration. - It does not significantly affect memories formed **before drug administration** (retrograde amnesia). *Anterograde amnesia* - Midazolam is well-known for its ability to induce **anterograde amnesia**, which is often a desirable effect in procedural sedation [2]. - This effect helps patients forget unpleasant or painful procedures performed while under its influence. *Causes tachyphylaxis during high dose infusions* - Prolonged or high-dose infusions of midazolam can lead to **tachyphylaxis**, requiring increased doses to achieve the same effect [1]. - This phenomenon is due to the **down-regulation or desensitization of GABA-A receptors** with continuous stimulation. *Decreased cardiovascular effects as compared to propofol* - Midazolam generally causes **less pronounced cardiovascular depression** (e.g., hypotension) compared to propofol, especially in standard sedative doses [1]. - This makes midazolam a safer option for sedation in some patients with **fragile cardiovascular statuses**.

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