What is the mechanism of action of Warfarin?
Which of the following anticoagulants is given orally?
What is Hydroxyethyl starch?
Which of the following is NOT an advantage of amoxicillin over ampicillin?
Which of the following conditions is not treated by penicillin G?
What is the mechanism of action of aminoglycoside antibiotics?
Which of the following statements about clofazimine is incorrect?
First generation cephalosporins are active against?
What is the most serious side effect associated with Raltegravir?
Mode of excretion of cyclophosphamide is?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 91: What is the mechanism of action of Warfarin?
- A. Inhibition of Vitamin K epoxide reductase (Correct Answer)
- B. Inhibition of gamma glutamyl carboxylase
- C. Activation of Vitamin K epoxide reductase
- D. Activation of gamma glutamyl carboxylase
Explanation: ***Inhibition of Vitamin K epoxide reductase*** - Warfarin blocks **Vitamin K epoxide reductase (VKORC1)** [1, 2, 3], an enzyme essential for recycling oxidized vitamin K into its active reduced form [1, 3]. - This reduction prevents the activation of **vitamin K-dependent clotting factors** (II, VII, IX, X), leading to anticoagulation [1, 3]. *Inhibition of gamma glutamyl carboxylase* - **Gamma-glutamyl carboxylase** uses reduced vitamin K as a cofactor to carboxylate specific glutamic acid residues on clotting factors [1, 3]. - While essential for clotting factor activation, this enzyme itself is **not directly inhibited by warfarin** [1, 3]. *Activation of Vitamin K epoxide reductase* - Activating **VKORC1** would increase the production of reduced vitamin K, thereby **promoting coagulation** rather than inhibiting it [1, 2]. - This is the opposite of warfarin's intended therapeutic effect. *Activation of gamma glutamyl carboxylase* - Activating **gamma-glutamyl carboxylase** would enhance the carboxylation and activation of **clotting factors**, leading to procoagulant effects [1, 3]. - This mechanism contradicts warfarin's role as an **anticoagulant**.
Question 92: Which of the following anticoagulants is given orally?
- A. Argatraban
- B. Alteplase
- C. Rivaroxaban (Correct Answer)
- D. Fondaparinux
Explanation: ***Rivaroxaban*** - Rivaroxaban is a **direct oral anticoagulant (DOAC)** that specifically inhibits **Factor Xa**. - It is administered orally and does not require routine coagulation monitoring. *Argatraban* - Argatroban is a **direct thrombin inhibitor (DTI)** primarily used intravenously, especially in patients with **heparin-induced thrombocytopenia (HIT)**. - It is not an orally administered anticoagulant. *Alteplase* - Alteplase is a **thrombolytic agent** (clot buster), not an anticoagulant, that works by converting **plasminogen to plasmin**. - It is administered intravenously to dissolve existing clots. *Fondaparinux* - Fondaparinux is a **synthetic pentasaccharide** that selectively inhibits **Factor Xa** by binding to antithrombin. - It is administered **subcutaneously**, not orally.
Question 93: What is Hydroxyethyl starch?
- A. Vasodilator
- B. Inotrope
- C. Plasma expander (Correct Answer)
- D. Diuretic
Explanation: ***Plasma expander*** - **Hydroxyethyl starch** is a **colloid solution** used intravenously to increase plasma volume and maintain oncotic pressure. - It is often used in situations of **hypovolemia** or shock to support circulation. *Vasodilator* - A **vasodilator** is a medication that widens blood vessels, typically used to lower blood pressure or improve blood flow. - Hydroxyethyl starch does not directly cause **vasodilation** as its primary mechanism of action. *Inotrope* - An **inotrope** is an agent that alters the force or energy of muscular contractions, mainly affecting the heart's contractility. - Hydroxyethyl starch has no direct effect on **myocardial contractility**. *Diuretic* - A **diuretic** is a substance that promotes increased production of urine, thereby increasing the excretion of water from the body. - While fluid administration can temporarily increase urine output, hydroxyethyl starch is not classified as a **diuretic agent** itself.
Question 94: Which of the following is NOT an advantage of amoxicillin over ampicillin?
- A. Spectrum includes H. influenzae & Shigella (Correct Answer)
- B. Incidence of diarrhea is lower
- C. Food does not interfere with its absorption
- D. Better bioavailability & faster action
Explanation: ***Spectrum includes H. influenzae & Shigella*** - Amoxicillin and ampicillin both have a similar spectrum of activity against *Haemophilus influenzae* and *Shigella* species. Neither drug possesses a distinct advantage over the other in this regard for these specific pathogens. - Therefore, stating that amoxicillin's spectrum *includes* these bacteria as an advantage over ampicillin implies a unique characteristic, which is incorrect. *Better bioavailability & faster action* - **Amoxicillin** has superior oral **bioavailability** compared to ampicillin, leading to higher and more consistent blood levels. - This improved absorption often translates to a **faster onset of action** and allows for less frequent dosing. *Incidence of diarrhea is lower* - **Amoxicillin** is associated with a **lower incidence of diarrhea** and other gastrointestinal side effects compared to ampicillin. - This is partly due to its better absorption, meaning less unabsorbed drug reaches the colon to disrupt normal flora. *Food does not interfere with its absorption* - The absorption of **amoxicillin is largely unaffected by food**, allowing it to be taken without regard to meals. - In contrast, ampicillin's absorption can be significantly reduced when taken with food, making amoxicillin more convenient.
Question 95: Which of the following conditions is not treated by penicillin G?
- A. Bacterial meningitis
- B. Syphilis
- C. Anthrax
- D. Rickettsial infection (Correct Answer)
Explanation: ***Rickettsial infection*** - **Rickettsial infections**, such as Rocky Mountain spotted fever or typhus, are caused by **obligate intracellular bacteria** that are not susceptible to penicillin G. - The primary treatment for rickettsial infections is **doxycycline**, due to its ability to penetrate host cells and inhibit bacterial protein synthesis. *Bacterial meningitis* - **Bacterial meningitis**, particularly caused by susceptible strains of *Neisseria meningitidis*, *Streptococcus pneumoniae*, and *Haemophilus influenzae*, can be effectively treated with **high-dose intravenous penicillin G** [1]. - Penicillin G's ability to cross the **blood-brain barrier** in inflamed meninges makes it a suitable option, though ceftriaxone is now more commonly used empirically due to resistance concerns [2]. *Syphilis* - **Penicillin G** remains the **drug of choice** for all stages of syphilis, caused by *Treponema pallidum*. - For primary, secondary, and early latent syphilis, a **single intramuscular dose of benzathine penicillin G** is curative. *Anthrax* - While **ciprofloxacin** and **doxycycline** are often considered first-line for anthrax, **penicillin G** can also be an effective treatment for susceptible strains of *Bacillus anthracis*. - It is particularly used in cases of less severe cutaneous anthrax or to de-escalate treatment once susceptibility is confirmed.
Question 96: What is the mechanism of action of aminoglycoside antibiotics?
- A. Inhibition of protein synthesis (Correct Answer)
- B. Inhibition of DNA replication
- C. Disruption of the cell membrane
- D. Inhibition of bacterial cell wall synthesis
Explanation: ***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.
Question 97: Which of the following statements about clofazimine is incorrect?
- A. Does not interfere with DNA synthesis (Correct Answer)
- B. Used in lepra reaction
- C. Used in treatment of leprosy
- D. Causes ichthyosis and hyperpigmentation
Explanation: ***Does not interfere with DNA synthesis*** - Clofazimine's primary mechanism of action involves **DNA binding** and **interference with bacterial DNA synthesis**. - It also generates **reactive oxygen species** and disrupts membrane function, contributing to its bactericidal effect. - **This statement is INCORRECT** - clofazimine does interfere with DNA synthesis. *Used in lepra reaction* - Clofazimine is a crucial component in the treatment of **leprosy**, particularly effective in managing **Type 2 lepra reactions (erythema nodosum leprosum)** due to its anti-inflammatory effects. - It helps to reduce the severity and duration of these acute inflammatory episodes. *Used in treatment of leprosy* - Clofazimine is a **core component of multidrug therapy (MDT) for leprosy**, particularly in multibacillary leprosy. - It is recommended by the **WHO** as part of the standard treatment regimen for leprosy. *Causes ichthyosis and hyperpigmentation* - Clofazimine commonly causes **hyperpigmentation of the skin, conjunctiva, and bodily fluids**, often appearing reddish-brown to black. - Less commonly, it can also lead to **ichthyosis (dry, scaly skin)** as a side effect.
Question 98: First generation cephalosporins are active against?
- A. Gram negative bacteria
- B. Gram positive bacteria (Correct Answer)
- C. Anaerobes
- D. Dermatophytes
Explanation: ***Gram positive bacteria*** - First-generation cephalosporins, such as **cefazolin** and **cephalexin**, primarily exhibit excellent activity against many **Gram-positive cocci**, including **staphylococci** and **streptococci**. - They are commonly used for skin and soft tissue infections and surgical prophylaxis due to this Gram-positive coverage. *Gram negative bacteria* - While first-generation cephalosporins have *some* activity against limited Gram-negative bacteria (e.g., *E. coli*, *Klebsiella pneumoniae*, *P. mirabilis*), their spectrum is generally weak and unreliable compared to later generations of cephalosporins. - They are not the drug of choice for serious Gram-negative infections. *Anaerobes* - First-generation cephalosporins have **poor activity** against most **anaerobic bacteria**. - For infections involving anaerobes, other antibiotics like **metronidazole**, **clindamycin**, or later-generation cephalosporins (e.g., cefoxitin, cefotetan) are generally preferred. *Dermatophytes* - Dermatophytes are **fungi** that cause skin, hair, and nail infections. - Cephalosporins are **antibacterial agents** and have **no activity** against fungi. Antifungal medications are required to treat dermatophyte infections.
Question 99: What is the most serious side effect associated with Raltegravir?
- A. Hyperglycemia
- B. Hypertension
- C. Headache
- D. Rhabdomyolysis (Correct Answer)
Explanation: ***Rhabdomyolysis*** - Raltegravir, an **integrase strand transfer inhibitor (INSTI)**, can cause muscle-related side effects, including **rhabdomyolysis** and **myopathy**. [2] - Patients may present with muscle pain, weakness, and elevated **creatine kinase (CK)** levels. *Headache* - While headache can be a general side effect of many medications, it is not a **distinguishing or severe adverse effect commonly associated with Raltegravir** that would require specific monitoring. - Other more prominent side effects are typically prioritized in counseling and monitoring for this drug. *Hyperglycemia* - **Hyperglycemia** is not a commonly reported or significant side effect of Raltegravir. - While some antiretrovirals, particularly certain **protease inhibitors (PIs)** and **nucleoside reverse transcriptase inhibitors (NRTIs)**, are associated with altered glucose metabolism, INSTIs like Raltegravir generally have a more favorable metabolic profile. [1] *Hypertension* - Hypertension is generally **not a recognized or common side effect** of Raltegravir. - Cardiovascular events and hypertension are more frequently associated with other classes of antiretroviral drugs or as comorbidities in HIV-positive patients, rather than directly with INSTIs.
Question 100: Mode of excretion of cyclophosphamide is?
- A. Lung
- B. Liver
- C. Kidney (Correct Answer)
- D. Skin
Explanation: ***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.