Emtricitabine is classified as which of the following?
Emtricitabine is a/an:
Which of the following combinations does not show synergistic action?
In patients undergoing INH therapy, which group is least likely to develop neuropathy?
Which of the following drugs is not used for the treatment of H. Pylori?
Which of the following is the longest acting carbapenem?
Which class of antihypertensive drugs is known to cause erectile dysfunction?
Which statement best describes first-order kinetics in pharmacokinetics?
Alkaline diuresis in drug poisoning is not done in?
Permission from DCGI [Drug controller general, India] is needed before which phase of drug trial?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 71: Emtricitabine is classified as which of the following?
- A. Alkylating agent
- B. Antimetabolite
- C. NRTI (Correct Answer)
- D. Integrase Inhibitor
Explanation: ***NRTI*** - Emtricitabine is a **nucleoside reverse transcriptase inhibitor (NRTI)**, a class of antiretroviral drugs used in the treatment of **HIV infection**. - As an NRTI, it works by inhibiting the enzyme **reverse transcriptase**, which is crucial for the HIV virus to replicate its RNA into DNA. *Alkylating agent* - Alkylating agents are a type of **chemotherapy drug** that kill cancer cells by damaging their DNA. - They are primarily used in **cancer treatment**, not for viral infections like HIV. *Antimetabolite* - Antimetabolites are drugs that interfere with DNA and RNA synthesis, often used in **chemotherapy** to treat cancer or in immunosuppression. - While they can inhibit nucleic acid synthesis, this is a broad category, and emtricitabine's specific mechanism and classification are as an NRTI. *Integrase Inhibitor* - Integrase inhibitors are another class of **antiretroviral drugs** that block the HIV enzyme integrase, preventing the viral DNA from integrating into the host cell's DNA. - While an antiretroviral, emtricitabine has a different mechanism of action and belongs to the NRTI class.
Question 72: Emtricitabine is a/an:
- A. Alkylating agent
- B. Mitotic inhibitor
- C. Nucleoside reverse transcriptase inhibitor (NRTI) (Correct Answer)
- D. None of the options
Explanation: ***Nucleoside reverse transcriptase inhibitor (NRTI)*** - **Emtricitabine** is a synthetic nucleoside analog that inhibits the activity of HIV-1 **reverse transcriptase**, an enzyme essential for viral replication. - It works by being phosphorylated to its active triphosphate form, which then competes with natural deoxycytidine triphosphate for incorporation into the viral DNA, leading to **chain termination**. *Alkylating agent* - **Alkylating agents** are a class of antineoplastic drugs that work by adding an alkyl group to DNA, forming a covalent bond that interferes with DNA replication and transcription. - They are primarily used in **cancer chemotherapy**, not as antiviral agents for HIV. *Mitotic inhibitor* - **Mitotic inhibitors** are drugs that interfere with cell division (mitosis) by targeting microtubules, either inhibiting their polymerization or depolymerization. - These agents are also used in **cancer treatment** to prevent rapidly dividing cells from completing mitosis. *None of the options* - This option is incorrect because **emtricitabine** clearly belongs to the class of **nucleoside reverse transcriptase inhibitors**.
Question 73: Which of the following combinations does not show synergistic action?
- A. Streptomycin plus penicillin
- B. Rifampicin plus dapsone
- C. Penicillin plus tetracycline (Correct Answer)
- D. Penicillin plus sulfonamide
Explanation: ***Penicillin plus tetracycline*** - This combination is generally **antagonistic** or **indifferent**, not synergistic. Penicillin is a cell wall synthesis inhibitor that works best on actively growing bacteria, while tetracycline is a bacteriostatic protein synthesis inhibitor that can reduce bacterial growth, thereby diminishing penicillin's effect. - The combination is usually avoided as the **bacteriostatic action of tetracycline** can counteract the **bactericidal action of penicillin**, leading to reduced efficacy, especially in infections requiring rapid bacterial clearance. *Penicillin plus sulfonamide* - This combination can show synergism in some contexts, particularly as sulfonamides inhibit **folate synthesis**, while penicillin inhibits **cell wall synthesis**. - While not a classic synergistic pair for all infections, their mechanisms of action are distinct, and they can sometimes be used together, although specific synergistic effects are more limited compared to other pairs. *Streptomycin plus penicillin* - This is a classic example of **synergistic action**, particularly in conditions like **enterococcal endocarditis**. - Penicillin damages the bacterial cell wall, allowing **streptomycin** (an aminoglycoside) to more easily penetrate the cell and act on ribosomal targets, leading to enhanced bactericidal effect. *Rifampicin plus dapsone* - This combination is a cornerstone of **multi-drug therapy for leprosy**, demonstrating clear synergy against *Mycobacterium leprae*. - **Rifampicin** inhibits bacterial RNA synthesis, and **dapsone** inhibits folate synthesis, attacking different essential bacterial pathways which, when combined, are more effective and reduce the development of resistance.
Question 74: In patients undergoing INH therapy, which group is least likely to develop neuropathy?
- A. Having malnutrition
- B. Alcoholics
- C. Fast acetylators (Correct Answer)
- D. Vitamin B complex deficiency
Explanation: ***Fast acetylators*** - **Fast acetylators** metabolize INH more quickly, leading to lower systemic drug levels and thus a reduced risk of adverse effects like neuropathy. - Neuropathy associated with INH is primarily due to **pyridoxine (vitamin B6) depletion**, which is less pronounced if the drug is rapidly cleared. *Having malnutrition* - **Malnutrition** often involves deficiencies in essential vitamins, including vitamin B6, which is crucial for preventing INH-induced neuropathy. - Patients with poor nutritional status are at a **higher risk** of developing neuropathy during INH therapy due to pre-existing vitamin B6 depletion. *Alcoholics* - **Alcoholism** is strongly associated with deficiencies in various B vitamins, particularly **pyridoxine (vitamin B6)**, due to poor diet and impaired absorption. - This pre-existing deficiency makes alcoholics **highly susceptible** to INH-induced neuropathy. *Vitamin B complex deficiency* - A **deficiency in vitamin B complex**, especially pyridoxine (B6), is a known risk factor for INH-induced neuropathy. - Isoniazid interferes with **pyridoxine metabolism**, and those with pre-existing deficiency are more vulnerable to this adverse effect.
Question 75: Which of the following drugs is not used for the treatment of H. Pylori?
- A. Bismuth
- B. Domperidone (Correct Answer)
- C. Clarithromycin
- D. Amoxicillin
Explanation: ***Correct: Domperidone*** - Domperidone is a **prokinetic drug** used to treat nausea, vomiting, and gastric motility disorders, but it has **no direct antibacterial activity** against *H. pylori*. - It works by blocking **dopamine receptors** in the chemoreceptor trigger zone and peripherally. - Therefore, it is **NOT used for *H. pylori* eradication**. *Incorrect: Bismuth* - **Bismuth subsalicylate** is a key component of **quadruple therapy** for *H. pylori* eradication, particularly in cases of antibiotic resistance or treatment failure. - It has **bactericidal effects** against *H. pylori*, disrupts its cell wall, and inhibits its adherence to the gastric mucosa. *Incorrect: Amoxicillin* - **Amoxicillin** is a penicillin-class antibiotic commonly used in various *H. pylori* eradication regimens, including **triple therapy**. - It acts by **inhibiting bacterial cell wall synthesis**, leading to bacterial lysis. *Incorrect: Clarithromycin* - **Clarithromycin** is a macrolide antibiotic frequently included in standard **triple therapy** for *H. pylori* eradication. - It inhibits **bacterial protein synthesis** by binding to the 50S ribosomal subunit.
Question 76: Which of the following is the longest acting carbapenem?
- A. Imipenem
- B. Meropenem
- C. Doripenem
- D. Ertapenem (Correct Answer)
Explanation: ***Ertapenem*** - **Ertapenem** has the **longest half-life** among the carbapenems, allowing for once-daily dosing. - Its prolonged action is due to its **chemical structure**, which provides high protein binding and reduced renal clearance compared to other carbapenems. *Imipenem* - **Imipenem** has a **relatively short half-life** and requires co-administration with cilastatin to prevent its renal metabolism by dehydropeptidase-1. - Its short duration of action necessitates **frequent dosing**, typically every 6 to 8 hours. *Meropenem* - **Meropenem** has a **shorter half-life** than ertapenem, generally requiring dosing every 8 hours. - Although it does not require cilastatin, its pharmacokinetic profile is not as extended as ertapenem's. *Doripenem* - **Doripenem** also has a **shorter half-life** than ertapenem, necessitating administration every 8 hours. - Its spectrum of activity is similar to meropenem, but it does not offer the same extended duration of action.
Question 77: Which class of antihypertensive drugs is known to cause erectile dysfunction?
- A. Calcium channel blocker
- B. ACE inhibitors
- C. AT1 receptor antagonists
- D. Beta-blockers (Correct Answer)
Explanation: ***Beta-blockers*** - **Beta-blockers** are the antihypertensive class most commonly associated with **erectile dysfunction** - Mechanism: Reduced cardiac output, decreased peripheral blood flow, central nervous system effects reducing libido, and blockade of β2-mediated vasodilation - **Non-selective beta-blockers** (propranolol, nadolol) have higher incidence of ED compared to selective β1-blockers (metoprolol, atenolol) - Newer vasodilating beta-blockers (nebivolol, carvedilol) have lower risk of sexual dysfunction *Calcium channel blockers* - Generally have **neutral or minimal effect** on erectile function - May even improve ED in some patients due to **vasodilatory properties** - Side effects include peripheral edema and headache, but not sexual dysfunction *ACE inhibitors* - Associated with **lower risk of erectile dysfunction** compared to other antihypertensives - May have neutral or even protective effects on sexual function - Preferred choice for hypertensive patients with existing sexual dysfunction concerns - Common side effects: dry cough and angioedema (not related to sexual function) *AT1 receptor antagonists* - **ARBs have neutral to potentially beneficial effects** on sexual function - Considered an excellent alternative for patients experiencing sexual side effects with other antihypertensive medications - Some studies suggest they may improve erectile function in hypertensive patients
Question 78: Which statement best describes first-order kinetics in pharmacokinetics?
- A. Absorption of the drug is independent of the serum concentration
- B. Elimination of the drug is proportional to the serum concentration (Correct Answer)
- C. Absorption of the drug is proportional to the serum concentration
- D. Elimination of the drug is independent of the serum concentration
Explanation: ***Elimination of the drug is proportional to the serum concentration*** - In **first-order kinetics**, a **constant fraction** (or percentage) of the drug is eliminated per unit of time. - This means that as the **serum drug concentration** increases, the absolute amount of drug eliminated per unit time also increases proportionally. *Absorption of the drug is independent of the serum concentration* - Drug absorption is generally driven by factors like **concentration gradient**, surface area, and blood flow, and while it can be influenced by drug concentration, this statement does not define first-order kinetics of *elimination*. - This statement is not the primary characteristic distinguishing first-order from zero-order kinetics regarding drug disposition. *Elimination of the drug is independent of the serum concentration.* - This describes **zero-order kinetics**, where a **constant amount** of drug is eliminated per unit of time, regardless of the serum concentration. - In zero-order kinetics, the elimination rate becomes saturated, so the elimination process cannot keep up with higher drug concentrations. *Absorption of the drug is proportional to the serum concentration* - While drug absorption can be proportional to the concentration (especially through passive diffusion), first-order kinetics specifically refers to the **elimination phase** of pharmacokinetics. - The rate of absorption can be a complex process and is not the defining characteristic for distinguishing first-order from zero-order *elimination*.
Question 79: Alkaline diuresis in drug poisoning is not done in?
- A. Aspirin
- B. Morphine (Correct Answer)
- C. Phenobarbitone
- D. Methotrexate
Explanation: ***Morphine*** - **Morphine** is an **alkaline drug**, so its elimination is actually enhanced by **acidification of the urine**, not alkalinization. - Alkaline diuresis would decrease the ionization of morphine in the renal tubules, leading to **increased reabsorption** and reduced excretion. *Aspirin* - **Aspirin (acetylsalicylic acid)** is an **acidic drug**, and **alkaline diuresis** is effective in increasing its excretion by trapping the ionized form in the renal tubules. - This process prevents reabsorption and promotes clearance, which is a standard treatment for aspirin overdose. *Methotrexate* - **Methotrexate** is a **weak organic acid**, and **alkaline diuresis** is crucial in reducing its toxicity, especially in high-dose therapy. - By increasing urine pH, the renal elimination of methotrexate is significantly enhanced, preventing kidney damage and systemic accumulation. *Phenobarbitone* - **Phenobarbitone** is a **weak acid**, and **alkaline diuresis** is a well-established method to increase its renal excretion in cases of overdose. - Alkalinization of the urine promotes the ionization of phenobarbitone, reducing its reabsorption by the renal tubules and accelerating its elimination.
Question 80: Permission from DCGI [Drug controller general, India] is needed before which phase of drug trial?
- A. Phase 1
- B. Phase 2
- C. Phase 3 (Correct Answer)
- D. Phase 4
Explanation: ***Phase 3*** - Permission from the **DCGI (Drug Controller General of India)** is mandatory before initiating **Phase 3** clinical trials as per **Schedule Y** of the Drugs and Cosmetics Rules. - Phase 3 trials involve **large-scale studies in Indian patients** to establish efficacy and safety in the target population, requiring explicit regulatory approval. - This is the critical regulatory checkpoint where DCGI evaluates the Phase 1 and 2 data before allowing widespread testing in Indian subjects. *Phase 1* - Phase 1 trials can be conducted after approval from the **Institutional Ethics Committee (IEC)** without requiring prior DCGI permission. - These trials in healthy volunteers focus on safety, pharmacokinetics, and dose-ranging studies. - DCGI is informed but explicit permission is not mandatory at this stage. *Phase 2* - Phase 2 trials also proceed with **IEC approval** and do not require prior DCGI permission. - These trials evaluate therapeutic efficacy and dose determination in a limited number of patients. - Results from Phase 2 are submitted to DCGI when seeking Phase 3 approval. *Phase 4* - Phase 4 trials are **post-marketing surveillance** studies conducted after drug approval. - These are conducted under the Post-Marketing Surveillance (PMS) framework. - While regulatory oversight exists, these are not pre-market trials requiring permission to initiate.