Which of the following is a parenteral direct thrombin inhibitor?
Which of the following drugs inhibits the activation of plasminogen?
Mechanism of action of tranexamic acid is
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?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 101: Which of the following is a parenteral direct thrombin inhibitor?
- A. Ximelagatran
- B. Dabigatran
- C. Argatroban (Correct Answer)
- D. Heparin
Explanation: ***Argatroban*** - **Argatroban** is a **synthetic direct thrombin inhibitor** administered exclusively via **intravenous infusion**, making it a parenteral drug. - It does not require antithrombin for its action and is primarily used in patients with **heparin-induced thrombocytopenia (HIT)**. *Ximelagatran* - **Ximelagatran** was an **oral direct thrombin inhibitor** but was withdrawn from the market due to concerns about severe **liver toxicity**. - As an oral drug, it is not a parenteral medication. *Dabigatran* - **Dabigatran** is a **direct thrombin inhibitor** that is administered **orally** in capsule form (as dabigatran etexilate, a prodrug). - Therefore, it is not a parenteral medication. *Heparin* - **Heparin** is an **indirect thrombin inhibitor** because it requires binding to **antithrombin** to exert its anticoagulant effect. - Although administered parenterally, its mechanism of action is indirect.
Question 102: Which of the following drugs inhibits the activation of plasminogen?
- A. Streptokinase
- B. Aminocaproic acid (Correct Answer)
- C. Reteplase
- D. Clopidogrel
Explanation: ***Correct Option: Aminocaproic acid*** - **Aminocaproic acid** is an antifibrinolytic drug that acts by competitively inhibiting the activation of **plasminogen** to plasmin. - By preventing the formation of plasmin, it stabilizes blood clots and is used to treat excessive bleeding. *Incorrect Option: Streptokinase* - **Streptokinase** is a **thrombolytic agent** that forms a complex with plasminogen, converting uncomplexed plasminogen into plasmin. - This action promotes the degradation of fibrin clots, making it a **fibrinolytic drug**, not an inhibitor of plasminogen activation. *Incorrect Option: Reteplase* - **Reteplase** is a **recombinant tissue plasminogen activator (tPA)** that directly converts plasminogen to plasmin. - This drug actively promotes **fibrinolysis** and clot breakdown, making it a thrombolytic agent. *Incorrect Option: Clopidogrel* - **Clopidogrel** is an **antiplatelet drug** that inhibits platelet aggregation by irreversibly blocking the P2Y12 adenosine diphosphate (ADP) receptor on platelets. - Its mechanism of action is focused on **platelet function**, not on the plasminogen-plasmin system.
Question 103: Mechanism of action of tranexamic acid is
- A. Decrease vascular permeability
- B. Smooth muscle contraction
- C. Activates Plasmin formation
- D. Prevents fibrinolysis (Correct Answer)
Explanation: ***Correct: Prevents fibrinolysis*** - Tranexamic acid is an **antifibrinolytic agent** that works by inhibiting the activation of plasminogen to plasmin. - By preventing the formation of plasmin, it stabilizes **fibrin clots** and reduces bleeding. *Incorrect: Decrease vascular permeability* - This is primarily the mechanism of action of drugs like antihistamines or corticosteroids, which work on **inflammation** and **allergic reactions**. - Tranexamic acid does not directly target vascular permeability; its primary role is in **hemostasis**. *Incorrect: Smooth muscle contraction* - This describes the action of drugs like **vasoconstrictors** (e.g., epinephrine) or agents that promote uterine contractions (e.g., oxytocin). - Tranexamic acid has no direct effect on **smooth muscle contraction**. *Incorrect: Activates Plasmin formation* - This is the opposite of tranexamic acid's action; drugs that activate plasmin, such as **tissue plasminogen activators (tPAs)**, are used to break down clots. - Tranexamic acid specifically **inhibits plasminogen activation**, thereby preventing plasmin formation.
Question 104: 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 105: 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 106: 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 107: 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 108: 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 109: 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 110: 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.