NEET-PG 2013 - Pharmacology Practice Questions

Q: Mechanism of action of tranexamic acid is

Prevents fibrinolysis. ***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.

Q: What is the mechanism of action of Warfarin?

Inhibition of Vitamin K epoxide reductase. ***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**.

Q: Which of the following anticoagulants is given orally?

Rivaroxaban. ***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.

Q: What is Hydroxyethyl starch?

Plasma expander. ***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.

Q: Which of the following is NOT an advantage of amoxicillin over ampicillin?

Spectrum includes H. influenzae & Shigella. ***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.

Q: Which of the following conditions is not treated by penicillin G?

Rickettsial infection. ***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.

Q: What is the mechanism of action of aminoglycoside antibiotics?

Inhibition of protein synthesis. ***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.

Q: Which of the following statements about clofazimine is incorrect?

Does not interfere with DNA synthesis. ***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.

Q: First generation cephalosporins are active against?

Gram positive bacteria. ***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.

Q: Which drug is commonly used to treat chronic hepatitis B infection?

Entecavir. ***Entecavir*** - **Entecavir** is an oral **nucleoside analog reverse transcriptase inhibitor** specifically approved and widely used for the treatment of **chronic hepatitis B virus (HBV) infection**. - It works by inhibiting HBV DNA polymerase, thereby reducing **viral replication** and preventing disease progression. *Atazanavir* - **Atazanavir** is a **protease inhibitor** primarily used in the treatment of **HIV infection**. - It is not indicated for the treatment of **hepatitis B virus infection**. *Zanamivir* - **Zanamivir** is a **neuraminidase inhibitor** used in the treatment and prevention of **influenza A and B viruses**. - It has no activity against **hepatitis B virus**. *Abacavir* - **Abacavir** is a **nucleoside reverse transcriptase inhibitor (NRTI)** used to treat **HIV infection**. - While it is an NRTI, it does not have significant efficacy against **hepatitis B virus** and is not used for its treatment.

Question 1

Mechanism of action of tranexamic acid is

Accepted Answer

Prevents fibrinolysis

Answer

Decrease vascular permeability

Answer

Smooth muscle contraction

Answer

Activates Plasmin formation

Question 2

What is the mechanism of action of Warfarin?

Accepted Answer

Inhibition of Vitamin K epoxide reductase

Answer

Inhibition of gamma glutamyl carboxylase

Answer

Activation of Vitamin K epoxide reductase

Answer

Activation of gamma glutamyl carboxylase

Question 3

Which of the following anticoagulants is given orally?

Accepted Answer

Rivaroxaban

Answer

Argatraban

Answer

Alteplase

Answer

Fondaparinux

Question 4

What is Hydroxyethyl starch?

Accepted Answer

Plasma expander

Answer

Vasodilator

Answer

Inotrope

Answer

Diuretic

Question 5

Which of the following is NOT an advantage of amoxicillin over ampicillin?

Accepted Answer

Spectrum includes H. influenzae & Shigella

Answer

Incidence of diarrhea is lower

Answer

Food does not interfere with its absorption

Answer

Better bioavailability & faster action

Question 6

Which of the following conditions is not treated by penicillin G?

Accepted Answer

Rickettsial infection

Answer

Bacterial meningitis

Answer

Syphilis

Answer

Anthrax

Question 7

What is the mechanism of action of aminoglycoside antibiotics?

Accepted Answer

Inhibition of protein synthesis

Answer

Inhibition of DNA replication

Answer

Disruption of the cell membrane

Answer

Inhibition of bacterial cell wall synthesis

Question 8

Which of the following statements about clofazimine is incorrect?

Accepted Answer

Does not interfere with DNA synthesis

Answer

Used in lepra reaction

Answer

Used in treatment of leprosy

Answer

Causes ichthyosis and hyperpigmentation

Question 9

First generation cephalosporins are active against?

Accepted Answer

Gram positive bacteria

Answer

Gram negative bacteria

Answer

Anaerobes

Answer

Dermatophytes

Question 10

Which drug is commonly used to treat chronic hepatitis B infection?

Accepted Answer

Entecavir

Answer

Zanamivir

Answer

Atazanavir

Answer

Abacavir

NEET-PG 2013 — Pharmacology