Pharmacology
10 questionsAmong the following statins, which has the longest half-life?
Which antitubercular drug makes the patient non-infective the earliest?
Thymidine is responsible for resistance to which antibiotic ?
Which of the following is not excreted by the kidney?
Which of the following is a primary use of Levamisole?
Quinine primarily acts on which stage of the Plasmodium life cycle?
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?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 421: Among the following statins, which has the longest half-life?
- A. Pravastatin
- B. Simvastatin
- C. Lovastatin
- D. Rosuvastatin (Correct Answer)
Explanation: **Rosuvastatin** - **Rosuvastatin** has the longest half-life among the commonly used statins, approximately **19 hours**, allowing for consistent lipid-lowering effects. - Its prolonged presence in the body contributes to its effectiveness in reducing **LDL-C** at lower doses. *Pravastatin* - **Pravastatin** has a relatively short half-life of about **1.8 hours**, requiring daily dosing to maintain therapeutic concentrations. - Its hydrophilic nature means it is less likely to penetrate non-hepatic tissues, potentially reducing extrahepatic side effects. *Simvastatin* - **Simvastatin** has a short half-life of about **3 hours**, necessitating daily administration. - It is a **prodrug** that requires hepatic activation to its active beta-hydroxy acid form. *Lovastatin* - **Lovastatin** also has a short half-life, around **3 hours**, and is a **prodrug** like simvastatin. - It is often recommended to be taken in the evening due to the diurnal rhythm of cholesterol synthesis.
Question 422: Which antitubercular drug makes the patient non-infective the earliest?
- A. Ethambutol
- B. Pyrazinamide
- C. Isoniazid (INH) (Correct Answer)
- D. Rifampin
Explanation: ***Isoniazid (INH)*** - **Isoniazid** renders TB patients **non-infectious the fastest**, typically within **2-3 days** of starting treatment - It has the most **rapid bactericidal effect** against actively multiplying extracellular **Mycobacterium tuberculosis**, which are the primary organisms responsible for transmission - INH works by inhibiting **mycolic acid synthesis**, disrupting the bacterial cell wall of rapidly dividing bacilli - This makes it the most critical drug for **early infection control** and reducing community transmission *Rifampin* - While **rifampin** is highly bactericidal and has excellent sterilizing activity, it takes **slightly longer** than INH to render patients non-infectious - Rifampin is particularly effective against **semi-dormant organisms** and intracellular bacilli - It is the most important drug for **preventing relapse** and shortening treatment duration, but INH acts faster in reducing infectivity *Ethambutol* - **Ethambutol** is primarily **bacteriostatic**, inhibiting arabinosyl transferase and interfering with cell wall synthesis - Its main role is to **prevent emergence of drug resistance** rather than rapidly reducing bacterial load - Has minimal impact on early infectivity reduction *Pyrazinamide* - **Pyrazinamide** is most effective against **semi-dormant bacilli** within macrophages and in acidic environments - Its **sterilizing activity** helps shorten overall treatment duration but does not contribute significantly to rapid reduction in infectivity - Works slowly and is not bactericidal against actively multiplying extracellular organisms
Question 423: Thymidine is responsible for resistance to which antibiotic ?
- A. Erythromycin
- B. Sulfonamide (Correct Answer)
- C. Tetracycline
- D. Nitrofurantoin
Explanation: ***Sulfonamide*** - **Thymidine** can contribute to **sulfonamide resistance** because sulfonamides interfere with **folate metabolism** and the subsequent synthesis of purines and pyrimidines, including thymidine. - An excess of thymidine can bypass the metabolic block caused by sulfonamides, allowing bacteria to continue DNA synthesis and grow. *Erythromycin* - **Erythromycin** resistance is primarily mediated by **methylation of ribosomal RNA**, which prevents the antibiotic from binding to the 50S ribosomal subunit. - It does not directly involve thymidine or the folate synthesis pathway. *Tetracycline* - Resistance to **tetracyclines** is commonly due to **efflux pumps** that actively pump the drug out of the bacterial cell or **ribosomal protection proteins** that prevent tetracycline binding. - Thymidine production or metabolism is not a mechanism of tetracycline resistance. *Nitrofurantoin* - **Nitrofurantoin** resistance typically involves **mutations** in bacterial enzymes (like **nitrofuran reductase**) that are responsible for activating the drug into its active form. - These mutations prevent the drug from becoming bactericidal, and thymidine does not play a role in this mechanism.
Question 424: Which of the following is not excreted by the kidney?
- A. Ciprofloxacin
- B. Ofloxacin
- C. Moxifloxacin (Correct Answer)
- D. Levofloxacin
Explanation: ***Moxifloxacin*** - Moxifloxacin is primarily metabolized in the **liver** and excreted through bile and feces. - This characteristic makes it a suitable choice for patients with significant **renal impairment** as dose adjustments are generally not required. *Ciprofloxacin* - Ciprofloxacin is predominantly excreted by the **kidneys** through both glomerular filtration and tubular secretion. - Dose adjustments are crucial in patients with **renal dysfunction** to prevent accumulation and toxicity. *Ofloxacin* - Ofloxacin is largely excreted unchanged in the **urine**, making renal excretion its primary elimination pathway. - **Dose reduction** is necessary for patients with impaired renal function. *Levofloxacin* - Levofloxacin is primarily eliminated via **renal excretion**, with a significant portion appearing in the urine as unmetabolized drug. - Patients with **kidney disease** require appropriate dose adjustments.
Question 425: Which of the following is a primary use of Levamisole?
- A. Immunostimulant
- B. Antihelminthic (Correct Answer)
- C. None of the options
- D. Immunomodulator
Explanation: ***Antihelminthic*** - Levamisole is **primarily classified as an antihelminthic drug**, used to treat parasitic worm infections. - It acts as a **nicotinic receptor agonist** in nematodes, causing spastic paralysis of the worms, leading to their expulsion. - It was historically used in humans for treating ascariasis and hookworm infections, and is still used in **veterinary medicine** for deworming livestock. - This is its **primary pharmacological classification** in standard medical textbooks. *Immunomodulator* - Levamisole does have **immunomodulatory properties** that were discovered secondary to its antihelminthic use. - It was used as **adjuvant therapy in colon cancer** (with 5-FU) to enhance immune response. - However, this is a **secondary use**, not its primary classification, and has been largely discontinued due to severe side effects like agranulocytosis. *Immunostimulant* - While levamisole can stimulate certain aspects of cell-mediated immunity, this overlaps with its immunomodulatory effects. - This is **not its primary pharmacological classification** - it remains primarily an antihelminthic agent. *None of the options* - This is incorrect because **antihelminthic** is clearly the primary and correct classification of levamisole in pharmacology. - Its antihelminthic action was its original and primary therapeutic application.
Question 426: Quinine primarily acts on which stage of the Plasmodium life cycle?
- A. Exoerythrocytic
- B. Pre-erythrocytic
- C. Erythrocytic (Correct Answer)
- D. None of the options
Explanation: ***Correct: Erythrocytic*** - Quinine primarily acts as a **blood schizonticide**, targeting the asexual erythrocytic stages of the *Plasmodium* parasite. - Its mechanism involves interfering with the parasite's ability to detoxify **heme**, leading to accumulation of toxic byproducts and parasite death within **red blood cells**. - This is why quinine is effective in treating **acute malaria attacks** during the symptomatic phase of the disease. *Incorrect: Exoerythrocytic* - The **exoerythrocytic stage** occurs in the liver, where sporozoites develop into merozoites. - Quinine has **minimal or no activity** against these liver stages, meaning it does not prevent initial infection or relapse from hepatic dormant forms (hypnozoites). - Drugs like **primaquine** target this stage. *Incorrect: Pre-erythrocytic* - The **pre-erythrocytic stage** is another term for the exoerythrocytic or liver stage of the parasite life cycle, occurring before the parasite enters red blood cells. - Medications that target this stage are known as **causal prophylactics**, which quinine is not. - Quinine has **no significant activity** at this stage. *Incorrect: None of the options* - This option is incorrect as quinine specifically targets the **erythrocytic stage**, making that option the correct answer. - Quinine's effectiveness in treating malaria stems from its action during the **symptomatic phase** of the disease, which corresponds to the erythrocytic cycle in red blood cells.
Question 427: 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 428: 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 429: 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 430: 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.