What is the drug of choice (DOC) for smoking cessation?
Imipenem, a newer antibiotic with a broad antibacterial spectrum, is co-administered with cilastatin. What is the primary reason for this combination?
Which among the following is most probable reason for preference of Cisatracurium over atracurium?
What is the drug of choice (DOC) for a scorpion sting bite?
Variation in sensitivity of response to different doses of a drug in different individuals is obtained from?
A drug with high plasma protein binding property has which of the following properties?
Which chemotherapy agents are commonly used for the treatment of retinoblastoma?
A 2-year-old boy weighing 12 kg is diagnosed with vitamin A deficiency. What is the recommended oral dose of vitamin A for him?
MgSO4 has no role in the prevention of...
What is the PRIMARY vascular function of PGI2 (prostacyclin)?
NEET-PG 2019 - Pharmacology NEET-PG Practice Questions and MCQs
Question 11: What is the drug of choice (DOC) for smoking cessation?
- A. Acamprosate
- B. Varenicline (Correct Answer)
- C. Thalidomide
- D. Tryptophan
Explanation: ***Varenicline*** - **Varenicline** is a **partial nicotinic receptor agonist** that reduces both the cravings for nicotine and the pleasurable effects of smoking. - It is considered a **first-line agent** for smoking cessation due to its effectiveness in increasing abstinence rates. *Acamprosate* - **Acamprosate** is a medication used to maintain abstinence from **alcohol dependence** by modulating GABA and glutamate neurotransmission. - It is **not indicated** for smoking cessation and has no direct mechanism of action related to nicotine addiction. *Thalidomide* - **Thalidomide** is an **immunomodulatory drug** with anti-angiogenic and anti-inflammatory properties, primarily used in conditions like **multiple myeloma** and **leprosy**. - It has **severe teratogenic effects** and is not used for smoking cessation due to its complex mechanism and significant side effect profile. *Tryptophan* - **Tryptophan** is an **essential amino acid** that serves as a precursor to **serotonin**, a neurotransmitter involved in mood regulation and sleep. - While it can impact mood, it is **not an approved or effective treatment** for directly addressing nicotine dependence or cravings.
Question 12: Imipenem, a newer antibiotic with a broad antibacterial spectrum, is co-administered with cilastatin. What is the primary reason for this combination?
- A. Cilastatin enhances the gastrointestinal absorption of imipenem.
- B. Cilastatin inhibits the beta-lactamase enzyme that degrades imipenem.
- C. Cilastatin prevents the degradation of imipenem by inhibiting an enzyme in the kidneys. (Correct Answer)
- D. The combination of antibiotics is synergistic against Pseudomonas species.
Explanation: ***Cilastatin prevents the degradation of imipenem by inhibiting an enzyme in the kidneys.*** - **Imipenem** is susceptible to degradation by **dehydropeptidase-1 (DHP-1)**, an enzyme found in the renal tubules, leading to inactivation and the production of potentially nephrotoxic metabolites. - **Cilastatin** is a **DHP-1 inhibitor** that prevents the inactivation of imipenem in the kidneys, thereby increasing its urinary concentration and reducing the risk of renal toxicity. *Cilastatin enhances the gastrointestinal absorption of imipenem.* - **Imipenem** is administered parenterally (intravenously) because it has **poor oral bioavailability** and is extensively metabolized in the gastrointestinal tract. - Cilastatin’s primary role is not to enhance GI absorption, as the drug is not intended for oral administration. *Cilastatin inhibits the beta-lactamase enzyme that degrades imipenem.* - **Imipenem** itself is highly resistant to most bacterial **beta-lactamase enzymes** due to its unique carbapenem structure. - Cilastatin does not have significant beta-lactamase inhibitory activity; its main function is renal enzyme inhibition. *The combination of antibiotics is synergistic against Pseudomonas species.* - While both imipenem and cilastatin together are effective due to preservation of imipenem, the combination itself is not a synergistic pair of antibiotics in the traditional sense against *Pseudomonas*. - Synergy typically refers to two different antibiotics working together, whereas cilastatin is an enzyme inhibitor, not an antibiotic.
Question 13: Which among the following is most probable reason for preference of Cisatracurium over atracurium?
- A. Decreased histamine release (Correct Answer)
- B. Increased histamine release
- C. Decreased CNS toxicity
- D. Due to elimination by non-specific plasma esterases
Explanation: ***Decreased histamine release*** - **Cisatracurium** is preferred over atracurium primarily due to its significantly **lower potential for histamine release**, which can cause undesirable side effects like **hypotension**, **tachycardia**, and **bronchospasm**. - This reduced histamine release contributes to a **more stable hemodynamic profile** and **fewer allergic-type reactions**, especially in critically ill or hemodynamically unstable patients. *Increased histamine release* - This is incorrect because **atracurium** is known to cause **more histamine release** compared to cisatracurium, which is why cisatracurium is often preferred. - Increased histamine release is an **undesirable effect** that can lead to adverse cardiovascular and respiratory reactions. *Decreased CNS toxicity* - While both drugs are **quaternary ammonium compounds** and do not readily cross the blood-brain barrier, **CNS toxicity** is not a primary concern or differentiating factor between atracurium and cisatracurium in clinical practice. - The potential for CNS effects from their metabolites (like **laudanosine**) is generally low with standard dosing, and **cisatracurium produces less laudanosine**. *Due to elimination by non-specific plasma esterases* - Both cisatracurium and atracurium are eliminated primarily by **Hofmann elimination** and **non-specific plasma esterases**. This is a shared characteristic, not a reason for cisatracurium's preference over atracurium. - **Hofmann elimination** is a non-enzymatic chemical degradation process that occurs at physiological pH and temperature, making their elimination **independent of renal or hepatic function**.
Question 14: What is the drug of choice (DOC) for a scorpion sting bite?
- A. EDTA
- B. Neostigmine
- C. N-acetylcysteine
- D. Prazosin (Correct Answer)
Explanation: ***Prazosin*** - **Prazosin** is an **alpha-1 adrenergic antagonist** that effectively counteracts the symptoms of scorpion envenomation, particularly **autonomic hyperactivity** like hypertension and tachycardia. - It works by blocking the effects of norepinephrine released by the scorpion venom, helping to stabilize vital signs and reduce cardiovascular complications. *EDTA* - **EDTA (ethylenediaminetetraacetic acid)** is a **chelating agent** primarily used to treat **heavy metal poisoning**, such as lead or mercury. - It binds to metal ions, forming a stable complex that can then be excreted from the body; it has no role in scorpion envenomation. *Neostigmine* - **Neostigmine** is an **acetylcholinesterase inhibitor** used to treat conditions like myasthenia gravis or to reverse the effects of neuromuscular blocking agents. - It increases acetylcholine levels at the neuromuscular junction; it is not indicated for the management of scorpion stings. *N-acetylcysteine* - **N-acetylcysteine (NAC)** is primarily used as an **antidote for acetaminophen overdose** and as a mucolytic agent in respiratory conditions. - It replenishes glutathione stores, helping to detoxify harmful metabolites; it has no direct role in treating scorpion venom effects.
Question 15: Variation in sensitivity of response to different doses of a drug in different individuals is obtained from?
- A. Dose-response relationship (Correct Answer)
- B. Therapeutic index
- C. Bioavailability
- D. Phase 1 clinical trials
Explanation: ***Dose-response relationship*** - The **dose-response relationship** (particularly the **graded dose-response curve**) describes how the magnitude of a drug's effect changes with different doses. - When plotted for different individuals or populations, these curves reveal **variation in sensitivity** through differences in potency (horizontal shift) and efficacy (maximum response). - This relationship helps characterize inter-individual variability in drug response and is the fundamental concept for understanding differential sensitivity. *Therapeutic index* - The **therapeutic index** is a measure of drug safety, representing the ratio between the toxic dose and the effective dose (TD50/ED50 or LD50/ED50). - It does not directly explain the variation in sensitivity to different doses among individuals, but rather provides information about the drug's overall safety margin. *Bioavailability* - **Bioavailability** refers to the fraction of an administered drug that reaches the systemic circulation unchanged. - While it influences the drug concentration at the site of action, it doesn't directly measure the variability in physiological response to that concentration among individuals. *Phase 1 clinical trials* - **Phase 1 clinical trials** are the first stage of testing a new drug in humans, primarily focusing on safety, dosage range, and pharmacokinetics in a small group of healthy volunteers. - While variability in response may be observed during these trials, they are not the *pharmacological concept* that describes this variation; rather, dose-response relationships are used to interpret findings from these trials.
Question 16: A drug with high plasma protein binding property has which of the following properties?
- A. Reduced renal clearance
- B. Less drug interaction
- C. Less tubular secretion
- D. Lower volume of distribution (Correct Answer)
Explanation: ***Lower volume of distribution*** - Drugs with high plasma protein binding are largely confined to the **vascular compartment** as they bind to proteins (e.g., albumin, alpha-1-acid glycoprotein), making them less available to distribute into tissues. - This confinement within the plasma compartment results in a **smaller apparent volume of distribution**. *Less drug interaction* - High plasma protein binding actually increases the potential for **drug-drug interactions** through displacement. - If a second drug displaces the first from its binding sites, it can increase the **free fraction** and potentially lead to toxicity. *Reduced renal clearance* - While highly protein-bound drugs are generally not easily filtered by the glomeruli, their primary route of elimination is often through **hepatic metabolism** or **active tubular secretion**, rather than reduced renal elimination. - Many highly protein-bound drugs still undergo significant renal excretion via **active secretion**, if they are substrates for active transporters. *Less tubular secretion* - Plasma protein binding does not inherently reduce tubular secretion; in some cases, the drug-protein complex can dissociate rapidly at the secretory sites, allowing for efficient secretion of the **free drug**. - In fact, many drugs that undergo significant tubular secretion are also highly protein-bound, as protein binding helps **maintain a concentration gradient** for and delivery of the drug to the secretion transporters.
Question 17: Which chemotherapy agents are commonly used for the treatment of retinoblastoma?
- A. vincristine, carboplatin and etoposide (Correct Answer)
- B. vinblastine, etoposide and bleomycin
- C. vinblastine, vincristine and etoposide
- D. vinblastine, vincristine and cisplatin
Explanation: ***Vincristine, carboplatin and etoposide*** - This combination is a well-established and commonly used **chemotherapy regimen** for the systemic treatment of retinoblastoma, particularly when there is significant intraocular disease or extraocular extension. - **Vincristine** targets microtubules, **carboplatin** is an alkylating agent, and **etoposide** is a topoisomerase inhibitor, working together to achieve a synergistic antineoplastic effect. *Vinblastine, etoposide and bleomycin* - While etoposide is used, **vinblastine** is not a primary agent for retinoblastoma, and **bleomycin** is more commonly associated with germ cell tumors or lymphomas, not retinoblastoma. - This combination lacks the broad spectrum of activity and specific targeting for retinoblastoma that is present in the standard regimen. *Vinblastine, vincristine and etoposide* - Although vincristine and etoposide are used, **vinblastine** is not typically included in the first-line systemic chemotherapy for retinoblastoma. - The absence of a platinum agent like carboplatin would make this regimen less effective for retinoblastoma, which often requires a strong alkylating agent. *Vinblastine, vincristine and cisplatin* - While vincristine is appropriate, **vinblastine** is not a standard component, and **cisplatin** is an alkylating agent but **carboplatin** is generally preferred in retinoblastoma due to its similar efficacy and a more favorable toxicity profile, especially regarding nephrotoxicity. - The use of cisplatin can lead to more significant **renal toxicity** and potentially ototoxicity compared to carboplatin, which is often avoided in a pediatric population when alternatives exist.
Question 18: A 2-year-old boy weighing 12 kg is diagnosed with vitamin A deficiency. What is the recommended oral dose of vitamin A for him?
- A. 200,000 I.U. (Correct Answer)
- B. 50,000 I.U.
- C. 100,000 I.U.
- D. 150,000 I.U.
Explanation: ***200,000 I.U.*** - According to **WHO guidelines**, for children aged **12 months and older** with vitamin A deficiency, the recommended oral dose is **200,000 I.U.** - This dose is given immediately upon diagnosis, repeated the next day, and a third dose is given 2-4 weeks later. - Since this child is **2 years old**, he falls into the ≥12 months category requiring 200,000 I.U. *100,000 I.U.* - A dose of **100,000 I.U.** is recommended for infants aged **6-11 months** with vitamin A deficiency. - This child is 2 years old, making 100,000 I.U. an insufficient dose for his age group. *50,000 I.U.* - A dose of **50,000 I.U.** is recommended for infants **younger than 6 months** diagnosed with vitamin A deficiency. - This dose is too low for a 2-year-old child. *150,000 I.U.* - **150,000 I.U.** is not a standard WHO-recommended dose for vitamin A deficiency treatment in any pediatric age group. - This is an incorrect dosing option.
Question 19: MgSO4 has no role in the prevention of...
- A. Bradycardia (Correct Answer)
- B. Seizures in severe pre-eclampsia
- C. Recurrent seizures in eclampsia
- D. Respiratory Distress Syndrome (RDS) in premature baby
Explanation: ***Bradycardia*** - Magnesium sulfate has **no role in preventing bradycardia**; in fact, it can **cause or worsen bradycardia** as a significant side effect. - MgSO4 acts as a **calcium channel blocker** and CNS depressant, which can lead to cardiac conduction depression and bradycardia. - Its administration requires careful monitoring for cardiorespiratory depression, including bradycardia. *Seizures in severe pre-eclampsia* - Magnesium sulfate is the **drug of choice** for prevention of eclamptic seizures in women with severe pre-eclampsia (Magpie Trial). - It acts as a **CNS depressant** by reducing acetylcholine release at the neuromuscular junction and inhibiting neuronal excitability. - Clear established role in seizure prophylaxis. *Recurrent seizures in eclampsia* - Magnesium sulfate is the **gold standard** for treatment of active eclamptic seizures and prevention of their recurrence. - Its **anticonvulsant properties** make it the first-line agent in managing this life-threatening complication of pregnancy. - Superior to other anticonvulsants like diazepam or phenytoin in this context. *Respiratory Distress Syndrome (RDS) in premature baby* - **Antenatal corticosteroids** (betamethasone/dexamethasone), NOT magnesium sulfate, are used for **prevention of RDS** in premature babies. - While MgSO4 given antenatally does provide **neuroprotection** and reduces risk of cerebral palsy in preterm infants, this is distinct from RDS prevention. - MgSO4 has no established role in preventing respiratory distress syndrome itself.
Question 20: What is the PRIMARY vascular function of PGI2 (prostacyclin)?
- A. Promotes platelet aggregation and causes vasoconstriction
- B. Acts primarily as a bronchoconstrictor
- C. Stimulates inflammatory cell chemotaxis
- D. Inhibits platelet aggregation and causes vasodilation (Correct Answer)
Explanation: ***Inhibits platelet aggregation and causes vasodilation*** - **PGI2 (prostacyclin)** is a potent **vasodilator** that relaxes smooth muscle in blood vessels, increasing blood flow. - It also effectively **inhibits platelet aggregation**, preventing the formation of blood clots. *Promotes platelet aggregation and causes vasoconstriction* - This describes the primary actions of **thromboxane A2 (TXA2)**, not PGI2. - TXA2 is produced by platelets and plays a key role in **hemostasis** by constricting blood vessels and promoting platelet clumping. *Acts primarily as a bronchoconstrictor* - While some prostaglandins can affect bronchial tone, **PGI2's primary vascular role** is vasodilation and anti-aggregation. - **Leukotrienes** and certain **prostaglandins (e.g., PGD2, PGF2α)** are more classically associated with bronchoconstriction. *Stimulates inflammatory cell chemotaxis* - This is primarily a function of other inflammatory mediators such as **leukotriene B4 (LTB4)** and **C5a anaphylatoxin**. - While other eicosanoids can indirectly influence inflammation, **PGI2's main actions** are vascular and anti-platelet.