What is an atypical side effect of montelukast?
Emtricitabine is a/an:
Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?
Ximelagatran is used as ?
What is the drug of choice for drug-induced peptic ulcer?
Among 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 a primary use of Levamisole?
Which of the following is not excreted by the kidney?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 11: What is an atypical side effect of montelukast?
- A. Goodpasture syndrome
- B. Membranous glomerulonephritis
- C. Bronchial asthma
- D. Churg-Strauss syndrome (Correct Answer)
Explanation: ***Churg-Strauss syndrome*** - The apparent development of **Churg-Strauss syndrome** (eosinophilic granulomatosis with polyangiitis) has been reported in patients treated with montelukast, although it is believed to be related more to the unmasking of the disease rather than a direct drug effect. - This typically occurs when **corticosteroids** are tapered or withdrawn as montelukast takes over, revealing the underlying vasculitis. *Goodpasture syndrome* - **Goodpasture syndrome** is an autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary hemorrhage, characterized by anti-glomerular basement membrane (GBM) antibodies. - There is no established association between montelukast use and the development of Goodpasture syndrome. *Membranous glomerulonephritis* - **Membranous glomerulonephritis** is a common cause of nephrotic syndrome, characterized by immune complex deposition on the glomerular basement membrane. - This condition is not typically linked to the use of montelukast. *Bronchial asthma* - **Bronchial asthma** is the condition montelukast is used to treat, acting as a leukotriene receptor antagonist to reduce inflammation and bronchoconstriction. - It is a primary indication for the drug, not a side effect.
Question 12: 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 13: Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?
- A. Low molecular weight heparin can also cause heparin-induced thrombocytopenia.
- B. Vitamin K is not an antidote for heparin-induced thrombocytopenia.
- C. Heparin-induced thrombocytopenia can occur after several days of heparin therapy.
- D. Antibodies are formed against heparin-platelet factor 4 complexes. (Correct Answer)
Explanation: **_Antibodies are formed against platelet factor 4._** - The underlying mechanism of **heparin-induced thrombocytopenia (HIT)** involves the formation of antibodies against complexes of **heparin and platelet factor 4 (PF4)** [2]. - These antibodies bind to the **heparin-PF4 complexes** on the surface of platelets, leading to platelet activation, aggregation, and consumption, which results in thrombocytopenia and a prothrombotic state [2]. *Low molecular weight heparin can also cause heparin-induced thrombocytopenia.* - While **low molecular weight heparin (LMWH)** has a lower incidence of causing HIT compared to unfractionated heparin, it can still trigger the condition [1], [2]. - This is because LMWH, like unfractionated heparin, can form complexes with PF4, leading to the same immune response in susceptible individuals [2]. *Vitamin K is not an antidote for heparin-induced thrombocytopenia.* - **Vitamin K** is the antidote for warfarin overdose, which works by reversing its anticoagulant effects [3]. - It has no role as an antidote for HIT because HIT is an **immune-mediated reaction** involving platelet activation, not a direct anticoagulant effect that can be reversed by Vitamin K [2]. *Heparin-induced thrombocytopenia can occur after several days of heparin therapy.* - HIT typically manifests after **5 to 10 days of heparin exposure**, as it takes time for the immune system to produce antibodies against the heparin-PF4 complexes [2]. - However, in patients with prior exposure to heparin, HIT can occur much sooner, even within **24 hours**, due to pre-existing antibodies.
Question 14: Ximelagatran is used as ?
- A. Anticoagulant (Correct Answer)
- B. Fibrinolytic
- C. Platelet inhibitor
- D. Clot buster
Explanation: ***Anticoagulant*** - Ximelagatran is a **direct thrombin inhibitor**, meaning it directly blocks the action of thrombin, a key enzyme in the coagulation cascade. - By inhibiting thrombin, it prevents the formation of **fibrin clots**, thus acting as an anticoagulant. *Platelet inhibitor* - **Platelet inhibitors** prevent platelets from clumping together to form a clot, often by targeting pathways like ADP receptors or COX-1 enzyme. - Examples include **aspirin** and **clopidogrel**, which have different mechanisms of action than Ximelagatran. *Clot buster* - **Clot busters** are also known as thrombolytic agents, which actively dissolve existing blood clots. - They work by activating **plasminogen** to produce plasmin, an enzyme that breaks down fibrin. *Fibrinolytic* - **Fibrinolytics** are a class of drugs that enhance **fibrinolysis**, the natural process of breaking down blood clots. - **Thrombolytics** are a subset of fibrinolytic drugs used therapeutically to dissolve clots.
Question 15: What is the drug of choice for drug-induced peptic ulcer?
- A. Prostaglandin analogues
- B. H2-receptor antagonists
- C. Proton pump inhibitors (Correct Answer)
- D. Antacids
Explanation: ***Proton pump inhibitors*** - **PPIs** are the most effective agents for treating and preventing **NSAID-induced peptic ulcers** by profoundly suppressing gastric acid secretion. - They provide **rapid symptom relief** and promote ulcer healing by creating an environment conducive to mucosal repair. *Prostaglandin analogues* - **Misoprostol**, a prostaglandin E1 analogue, can prevent NSAID-induced ulcers, but its use is limited by **gastrointestinal side effects** such as diarrhea and abdominal cramping. - While they protect the gastric mucosa, their efficacy in healing established ulcers is generally **inferior to PPIs**. *H2-receptor antagonists* - **H2-blockers** are effective in reducing gastric acid, but they are **less potent** than PPIs and typically do not heal **gastric ulcers** as effectively, especially those induced by NSAIDs. - They are more commonly used for preventing **duodenal ulcers** and managing symptoms of GERD. *Antacids* - Antacids provide **immediate, temporary relief** of ulcer symptoms by neutralizing existing stomach acid. - They do not address the underlying pathology or promote **ulcer healing** and are therefore not considered the drug of choice for treatment.
Question 16: 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 17: 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 18: 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 19: 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 20: 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.