NEET-PG 2013 - Pharmacology Practice Questions

Q: Muscarinic cholinergic receptors are seen at all sites, except?

Neuromuscular junction. ***Neuromuscular junction*** - The **neuromuscular junction** primarily contains **nicotinic cholinergic receptors**, not muscarinic receptors. - Activation of these nicotinic receptors by acetylcholine causes muscle contraction. *Stomach* - The stomach contains **muscarinic M3 receptors** which mediate gastric acid secretion and smooth muscle contraction. - Activation by acetylcholine via the vagus nerve promotes digestion. *CNS* - The **central nervous system** has various subtypes of **muscarinic receptors (M1-M5)** distributed throughout, playing roles in learning, memory, and motor control. - These receptors modulate neuronal excitability and neurotransmitter release. *Glands* - Most exocrine glands (e.g., salivary, lacrimal, sweat glands) are richly supplied with **muscarinic receptors**, primarily **M3**. - Activation leads to increased glandular secretion.

Q: Which dopamine receptor is known for its inhibitory action in the central nervous system?

Dopamine Receptor D2. ***Dopamine Receptor D2*** - The **D2 receptor** is a member of the D2-like family (D2, D3, D4), which are **G-protein coupled receptors** that inhibit adenylyl cyclase activity. - Its activation typically leads to a **decrease in neuronal excitability** and neurotransmitter release, providing an inhibitory effect in the CNS. *Dopamine Receptor D5* - The **D5 receptor** belongs to the D1-like family (D1, D5), which are **G-protein coupled receptors** that stimulate adenylyl cyclase activity. - Activation of D5 receptors typically leads to **excitatory effects** rather than inhibitory ones in the CNS. *No inhibitory dopamine receptor present* - This statement is incorrect as specific dopamine receptor subtypes, particularly the **D2-like family**, are well-established to exert inhibitory actions in the CNS. - These inhibitory effects are crucial for various physiological processes, including motor control and reward pathways. *Dopamine Receptor D1* - The **D1 receptor** is part of the D1-like family (D1, D5) and is known for its **excitatory effects** in the CNS. - Activation of D1 receptors leads to an **increase in intracellular cAMP** and generally enhances neuronal activity.

Q: 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?

Physiological antagonism. ***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.

Q: Which of the following is a metabolite of hydroxyzine?

Cetirizine. ***Cetirizine*** - **Cetirizine** is the principal active metabolite of **hydroxyzine**, formed through the oxidation of the primary alcohol group of hydroxyzine [2]. - Both hydroxyzine and cetirizine are **H1-receptor antagonists**, but cetirizine is a **second-generation antihistamine** known for being less sedating due to its limited ability to cross the blood-brain barrier [2]. *Fexofenadine* - **Fexofenadine** is an active metabolite of **terfenadine**, not hydroxyzine [2]. - **Fexofenadine** is a second-generation antihistamine used to treat allergies, known for its non-sedating properties [3]. *Terfenadine* - **Terfenadine** is a second-generation antihistamine that was withdrawn from the market due to its cardiotoxicity, particularly the risk of **QT prolongation** and **Torsades de Pointes**. - Its active metabolite is **fexofenadine**, which does not cause similar cardiac issues [2]. *Azelastine* - **Azelastine** is an antihistamine primarily available as a **nasal spray** for the treatment of allergic rhinitis and conjunctivitis [1], [3]. - It is not a metabolite of hydroxyzine but a distinct therapeutic compound.

Q: What is the mechanism of action of aminoglycoside antibiotics?

Inhibition of protein synthesis. ***Inhibition of protein synthesis*** - Aminoglycosides **bind irreversibly to the 30S ribosomal subunit** of bacteria, interfering with the initiation complex formation and causing misreading of mRNA. - This leads to the production of **non-functional proteins** and ultimately bacterial cell death, making them bactericidal. *Disruption of the cell membrane* - This mechanism is characteristic of **polymyxins** (e.g., colistin), which interact with bacterial cell membranes, increasing permeability and causing leakage of intracellular contents. - Aminoglycosides do not primarily target the cell membrane for their bactericidal action. *Inhibition of DNA replication* - This mechanism is associated with **fluoroquinolones**, which inhibit bacterial topoisomerase II (DNA gyrase) and topoisomerase IV. - Aminoglycosides do not interfere with DNA synthesis or replication. *Inhibition of bacterial cell wall synthesis* - This is the mechanism of action for **beta-lactam antibiotics** (e.g., penicillins, cephalosporins) and **glycopeptides** (e.g., vancomycin), which target peptidoglycan synthesis. - Aminoglycosides do not affect the bacterial cell wall but rather their intracellular protein machinery.

Q: Mode of excretion of cyclophosphamide is?

Kidney. ***Kidney*** - Cyclophosphamide is a **prodrug** that undergoes metabolism in the liver to its active forms. However, both the parent drug and its active metabolites are primarily **excreted renally**. [1] - Renal excretion means that patients with **renal impairment** may require dose adjustments to prevent drug accumulation and increased toxicity. [3] *Lung* - The lungs are primarily involved in **gas exchange** and the elimination of volatile substances, not non-volatile drugs like cyclophosphamide. - While some drugs can be excreted to a minor extent via the lungs, it is not the primary route for **cyclophosphamide**. *Liver* - The liver is the primary site of **metabolism** for cyclophosphamide, where it is converted into active cytotoxic metabolites. [1], [2] - While metabolites are formed here, the liver is not the main organ for the final **elimination** (excretion) of the drug or its metabolites from the body. *Skin* - The skin's role in drug excretion is generally minimal, mainly involving substances excreted in **sweat**, and is not a significant route for cyclophosphamide. - Excretion via the skin is typically very limited for most drugs and does not play a major role in the elimination of **chemotherapeutic agents** like cyclophosphamide.

Q: An Englishman travels to a place which is resistant to chloroquine and mefloquine. What should he take as prophylaxis?

Atovaquone-proguanil. ***Atovaquone-proguanil*** - This combination, known as **Malarone**, is the most appropriate prophylactic agent for areas with **multi-drug resistant malaria**, including resistance to chloroquine and mefloquine [1], [2]. - It targets multiple stages of the parasite life cycle, providing excellent protection and is generally well-tolerated with specific **WHO and CDC recommendations** for chloroquine and mefloquine resistant areas [1], [3]. *Primaquine* - **Primaquine** is primarily used for **causal prophylaxis** against *P. vivax* and *P. ovale* to prevent relapse, not as primary prophylaxis [2]. - It is not typically recommended as the primary prophylactic agent in areas with **chloroquine and mefloquine resistance** and requires **G6PD testing** due to risk of hemolysis [1]. *Proguanil* - While proguanil is used for malaria prophylaxis, **proguanil alone** is not effective enough for prophylaxis in areas with multi-drug resistant malaria. - It is typically used in **combination with atovaquone** rather than as monotherapy for effective protection [3]. *Doxycycline* - **Doxycycline** is also an effective prophylactic agent for areas with **chloroquine and mefloquine-resistant malaria** and is commonly recommended [1], [2]. - While effective, it can cause **photosensitivity** and **gastrointestinal upset**, making atovaquone-proguanil the preferred first-line choice.

Q: What is the initial loading dose of chloroquine base for treating uncomplicated malaria in children?

10 mg/kg (maximum 600 mg). ***10 mg/kg (maximum 600 mg)*** - The standard **initial loading dose** of chloroquine base for uncomplicated malaria in children is **10 mg/kg body weight**, with a maximum cap of **600 mg** to prevent toxicity. - This is followed by **5 mg/kg** at 6 hours, 24 hours, and 48 hours (total course of 25 mg/kg over 3 days). - This represents **WHO-recommended** weight-based dosing for pediatric malaria treatment. *5 mg/kg* - **5 mg/kg** is the dose for the **subsequent doses** (at 6, 24, and 48 hours after the initial dose), not the initial loading dose. - The initial dose must be higher (10 mg/kg) to rapidly achieve therapeutic blood levels. *15 mg/kg* - **15 mg/kg** exceeds the recommended initial dose and increases the risk of **chloroquine toxicity**. - Chloroquine has a narrow therapeutic index, and overdosing can cause serious **cardiovascular** (arrhythmias, hypotension) and **neurological** effects (seizures, visual disturbances). *25 mg/kg* - **25 mg/kg** represents the **total cumulative dose** over the entire 3-day treatment course, not the initial single dose. - Giving this amount as a single dose would result in severe toxicity and is contraindicated.

Q: Why do NSAIDs cause gastric ulcers?

They inhibit COX-1 and COX-2 enzymes. ***They inhibit COX-1 and COX-2 enzymes*** - NSAIDs primarily exert their anti-inflammatory effects by inhibiting **cyclooxygenase (COX) enzymes**, specifically COX-1 and COX-2. - While COX-2 inhibition is responsible for anti-inflammatory action, **COX-1 inhibition** reduces the production of protective prostaglandins in the gastric mucosa, leading to a loss of mucosal integrity and an increased risk of ulceration. *They inhibit the production of protective mucus* - While NSAIDs do compromise the gastric mucosal barrier, their primary mechanism is not a direct inhibition of mucus production itself. - Instead, the reduced prostaglandin synthesis indirectly affects the quantity and quality of mucus and bicarbonate, which are crucial for mucosal defense. *They increase gastric acid secretion* - NSAIDs do not directly increase gastric acid secretion; in fact, some studies suggest a mild inhibitory effect. - The main problem is the diminished mucosal protection against the normal levels of gastric acid. *They delay gastric emptying* - Delaying gastric emptying is not a primary mechanism by which NSAIDs cause ulcers. - While some medications can affect gastric motility, this is not the key pathway for NSAID-induced gastropathy.

Q: Which drug is primarily used in the treatment of breast cancer?

Tamoxifen. ***Tamoxifen*** - **Tamoxifen** is a **selective estrogen receptor modulator (SERM)** primarily used to treat and prevent **estrogen receptor (ER)-positive breast cancer**. - It works by blocking estrogen from binding to receptors in breast cancer cells, thereby inhibiting their growth. *Cyproterone* - **Cyproterone** is an **anti-androgen** and **progestogen** primarily used to treat conditions like **prostate cancer**, **acne**, and **hirsutism** in women. - Its main mechanism involves blocking androgen receptors and reducing androgen production, which is not the primary pathway for breast cancer. *Testosterone* - **Testosterone** is an **androgen** (male sex hormone) and is **not used** in the primary treatment of breast cancer. - In certain rare cases of severe metastatic breast cancer, androgens like high-dose testosterone have been historically used for palliation, but this is not standard therapy. *Chlorambucil* - **Chlorambucil** is an **alkylating agent** used primarily in the treatment of **chronic lymphocytic leukemia (CLL)** and certain **lymphomas**. - It works by interfering with DNA replication and transcription, but it is not a first-line or primary agent for breast cancer.

Question 1

Muscarinic cholinergic receptors are seen at all sites, except?

Accepted Answer

Neuromuscular junction

Answer

Stomach

Answer

CNS

Answer

Glands

Question 2

Which dopamine receptor is known for its inhibitory action in the central nervous system?

Accepted Answer

Dopamine Receptor D2

Answer

Dopamine Receptor D5

Answer

No inhibitory dopamine receptor present

Answer

Dopamine Receptor D1

Question 3

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?

Accepted Answer

Physiological antagonism

Answer

Chemical antagonism

Answer

Reversible antagonism

Answer

Competitive antagonism

Question 4

Which of the following is a metabolite of hydroxyzine?

Accepted Answer

Cetirizine

Answer

Fexofenadine

Answer

Terfenadine

Answer

Azelastine

Question 5

What is the mechanism of action of aminoglycoside antibiotics?

Accepted Answer

Inhibition of protein synthesis

Answer

Inhibition of DNA replication

Answer

Disruption of the cell membrane

Answer

Inhibition of bacterial cell wall synthesis

Question 6

Mode of excretion of cyclophosphamide is?

Accepted Answer

Kidney

Answer

Lung

Answer

Liver

Answer

Skin

Question 7

An Englishman travels to a place which is resistant to chloroquine and mefloquine. What should he take as prophylaxis?

Accepted Answer

Atovaquone-proguanil

Answer

Primaquine

Answer

Doxycycline

Answer

Proguanil

Question 8

What is the initial loading dose of chloroquine base for treating uncomplicated malaria in children?

Accepted Answer

10 mg/kg (maximum 600 mg)

Answer

5 mg/kg

Answer

15 mg/kg

Answer

25 mg/kg

Question 9

Why do NSAIDs cause gastric ulcers?

Accepted Answer

They inhibit COX-1 and COX-2 enzymes

Answer

They increase gastric acid secretion

Answer

They delay gastric emptying

Answer

They inhibit the production of protective mucus

Question 10

Which drug is primarily used in the treatment of breast cancer?

Accepted Answer

Tamoxifen

Answer

Cyproterone

Answer

Testosterone

Answer

Chlorambucil

NEET-PG 2013 — Pharmacology