NEET-PG 2015 Practice Questions

Q: Which of the following medications is classified as a stool softener?

Docusates. **Docusates** - **Docusates** (e.g., docusate sodium, docusate calcium) are **stool softeners** that work by reducing the surface tension of stool, allowing water and lipids to penetrate. - This increases the water content in the stool, making it softer and easier to pass, which is particularly useful in preventing straining after surgery or in conditions like hemorrhoids. *Bran* - **Bran** is a **bulk-forming laxative**, a type of dietary fiber that adds mass to the stool. - It absorbs water in the intestines, which increases stool volume and stimulates bowel movements, but it does not directly soften the stool in the same way docusates do. *Senna* - **Senna** is a **stimulant laxative** that works by irritating the bowel wall to promote peristalsis and bowel evacuation. - While it can help move stool, it does not act primarily by softening it, and prolonged use can lead to dependency or electrolyte imbalances. *Phenolphthalein* - **Phenolphthalein** is a **stimulant laxative** that was historically used to promote bowel movements. - It is no longer widely used due to concerns about potential carcinogenicity and other adverse effects, and it does not function as a stool softener.

Q: What is the drug of choice for drug-induced peptic ulcer?

Proton pump inhibitors. ***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.

Q: Ximelagatran is used as ?

Anticoagulant. ***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.

Q: Which of the following is a characteristic of simvastatin?

Derived from fungal metabolite. ***Derived from fungal metabolite*** - **Simvastatin** and lovastatin are **naturally-derived statins** obtained from **fungal metabolites** (*Aspergillus terreus*), distinguishing them from synthetic statins like atorvastatin, rosuvastatin, and pravastatin [2]. - This is the **most distinguishing characteristic** for classification purposes, as it represents the drug's origin and places it in a specific subclass of HMG-CoA reductase inhibitors. - The discovery of fungal-derived statins led to the development of the entire statin drug class. *Prodrug requiring hepatic activation* - While **simvastatin** is a **lactone prodrug** requiring hepatic hydrolysis to its active beta-hydroxy acid form, this is a pharmacokinetic property shared with lovastatin [1]. - This is a characteristic but not the most distinguishing feature for classification. *Specific CYP3A4 substrate with high interaction potential* - **Simvastatin** is extensively metabolized by **CYP3A4**, leading to significant drug-drug interactions with CYP3A4 inhibitors (e.g., ketoconazole, erythromycin, grapefruit juice). - While clinically important, many drugs are CYP3A4 substrates, making this less distinctive as a defining characteristic. *Short half-life requiring evening dosing* - **Simvastatin** has a **short half-life** (2-3 hours) and is preferably administered in the evening because cholesterol synthesis is highest at night. - This is a dosing consideration based on pharmacokinetics rather than a fundamental distinguishing characteristic of the drug's identity.

Q: Among the following statins, which has the longest half-life?

Rosuvastatin. **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.

Q: Which antitubercular drug makes the patient non-infective the earliest?

Isoniazid (INH). ***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

Q: Thymidine is responsible for resistance to which antibiotic ?

Sulfonamide. ***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.

Q: Which of the following is not excreted by the kidney?

Moxifloxacin. ***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.

Q: Which of the following is a primary use of Levamisole?

Antihelminthic. ***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.

Q: Rebound increase in gastric acid secretion after stopping proton pump inhibitor therapy is due to?

Hypergastrinemia. ***Hypergastrinemia*** - Proton pump inhibitors (PPIs) create a state of **hypochlorhydria** (reduced stomach acid), which in turn stimulates the **G cells** in the stomach to produce more **gastrin**. - This elevated gastrin level leads to a compensatory increase in the number and activity of **parietal cells**, causing a rebound hypersecretion of acid when PPI therapy is discontinued. *Parietal cell hyperplasia* - While parietal cell hyperplasia can occur, it is a consequence of chronic **hypergastrinemia**, not the primary driver of rebound acid secretion. - The direct effect of increased gastrin stimulating existing parietal cells is more immediate and significant for the rebound phenomenon. *Increased histamine release* - Elevated histamine release from **enterochromaffin-like (ECL) cells** is a downstream effect of hypergastrinemia, as gastrin stimulates ECL cells. - While increased histamine contributes to acid secretion, the root cause for its increase in this context is the **hypergastrinemia** induced by PPIs. *Hypersensitivity of Ach receptors* - **Acetylcholine (Ach) receptors** on parietal cells are involved in direct neural stimulation of acid secretion. - There is no evidence that stopping PPIs causes an increased sensitivity of these receptors, or that this is the primary mechanism of rebound acid secretion.

Question 1

Which of the following medications is classified as a stool softener?

Accepted Answer

Docusates

Answer

Bran

Answer

Senna

Answer

Phenolphthalein

Question 2

What is the drug of choice for drug-induced peptic ulcer?

Accepted Answer

Proton pump inhibitors

Answer

Prostaglandin analogues

Answer

H2-receptor antagonists

Answer

Antacids

Question 3

Ximelagatran is used as ?

Accepted Answer

Anticoagulant

Answer

Fibrinolytic

Answer

Platelet inhibitor

Answer

Clot buster

Question 4

Which of the following is a characteristic of simvastatin?

Accepted Answer

Derived from fungal metabolite

Answer

Specific CYP3A4 substrate with high interaction potential

Answer

Prodrug requiring hepatic activation

Answer

Short half-life requiring evening dosing

Question 5

Among the following statins, which has the longest half-life?

Accepted Answer

Rosuvastatin

Answer

Pravastatin

Answer

Simvastatin

Answer

Lovastatin

Question 6

Which antitubercular drug makes the patient non-infective the earliest?

Accepted Answer

Isoniazid (INH)

Answer

Ethambutol

Answer

Pyrazinamide

Answer

Rifampin

Question 7

Thymidine is responsible for resistance to which antibiotic ?

Accepted Answer

Sulfonamide

Answer

Erythromycin

Answer

Tetracycline

Answer

Nitrofurantoin

Question 8

Which of the following is not excreted by the kidney?

Accepted Answer

Moxifloxacin

Answer

Ciprofloxacin

Answer

Ofloxacin

Answer

Levofloxacin

Question 9

Which of the following is a primary use of Levamisole?

Accepted Answer

Antihelminthic

Answer

Immunostimulant

Answer

None of the options

Answer

Immunomodulator

Question 10

Rebound increase in gastric acid secretion after stopping proton pump inhibitor therapy is due to?

Accepted Answer

Hypergastrinemia

Answer

Parietal cell hyperplasia

Answer

Increased histamine release

Answer

Hypersensitivity of Ach receptors

NEET-PG 2015

Pharmacology

Physiology