NEET-PG 2012 - Pharmacology Practice Questions

Q: Romiplostim mimics which of the following receptors?

Thrombopoietin. ***Thrombopoietin*** - **Romiplostim** is a **thrombopoietin receptor agonist**, meaning it binds to and activates the **thrombopoietin receptor** [1]. - This activation mimics the effect of endogenous thrombopoietin, stimulating the production of **platelets** in the bone marrow [2].*IL 6* - **Interleukin-6 (IL-6)** is a cytokine involved in inflammation, immune response, and hematopoiesis, but it is not the primary target of romiplostim. - While IL-6 can influence platelet production indirectly, romiplostim directly targets the thrombopoietin pathway.*IL 8* - **Interleukin-8 (IL-8)** is a chemokine primarily involved in neutrophil chemotaxis and inflammation. - It plays no direct role in the mechanism of action of romiplostim.*PGE 1* - **Prostaglandin E1 (PGE1)** is a lipid compound with various effects, including vasodilation and inhibition of platelet aggregation. - Romiplostim's mechanism of action is distinct from that of prostaglandins, as it specifically targets platelet production rather than platelet function or vascular tone.

Q: Sulphonamide injection causes decrease in folic acid by?

Inhibition through competition with substrate. ***Inhibition through competition with substrate***Sulphonamides are **structural analogs of p-aminobenzoic acid (PABA)**, a substrate crucial for dihydropteroate synthase [1, 2]. They competitively inhibit this enzyme, which synthesizes **dihydrofolic acid**, a precursor to **tetrahydrofolic acid (THF)**, thereby reducing folic acid production in bacteria [1, 2].*Inhibition without competition*This typically refers to **non-competitive inhibition**, where the inhibitor binds to an allosteric site and changes the enzyme's conformation, regardless of substrate concentration. Sulphonamides, however, specifically compete with PABA at the active site of **dihydropteroate synthase**.*Inhibition through a different site*This describes **allosteric inhibition** or non-competitive inhibition, where the inhibitor binds to a site other than the active site. Sulphonamides do not work through an allosteric mechanism; they directly interfere with the binding of PABA at the enzyme's active site.*Inhibition that does not involve the active site*This is another way to describe **non-competitive** or **allosteric inhibition**, where the inhibitor binds elsewhere on the enzyme, altering its function without directly blocking the active site. Sulphonamides' mechanism is distinct, as they closely resemble the natural substrate and directly compete for the active site of **dihydropteroate synthase**.

Q: Which of the following is the most common side effect of Cimetidine?

CNS effects (confusion, dizziness). ***CNS effects (confusion, dizziness)*** - **Cimetidine** is a **H2-receptor antagonist** that can cross the **blood-brain barrier**, leading to **central nervous system (CNS) side effects**. - These effects, including **confusion, dizziness**, and **headache**, are more common in elderly patients or those with renal impairment due to reduced drug clearance. *Impotence* - While **cimetidine** can cause **endocrine effects** due to its anti-androgenic activity, **impotence** is a less common side effect compared to CNS disturbances. - It results from the drug's interference with **testosterone metabolism** and binding to **androgen receptors**. *Gynaecomastia* - **Gynaecomastia** is a known **endocrine side effect** of **cimetidine** due to its **anti-androgenic activity** and promotion of **prolactin release**. - However, CNS side effects are generally encountered more frequently in clinical practice. *Diarrhea* - **Gastrointestinal side effects** like **diarrhea** are possible with various medications, but they are not the most common or characteristic side effect of **cimetidine**. - Nausea and constipation are also reported, but generally less frequently than CNS effects.

Q: Which of the following is an intermediate-acting insulin?

NPH insulin. ***NPH insulin*** - **NPH (Neutral Protamine Hagedorn) insulin** is characterized by its intermediate duration of action, typically peaking in 4-12 hours and lasting up to 24 hours [1]. - This intermediate profile is achieved by combining insulin with **protamine**, which slows its absorption from the subcutaneous injection site [1]. *Insulin lispro* - **Insulin lispro** is a **rapid-acting insulin** analog, designed to act very quickly after injection, typically within 15-30 minutes [1, 2]. - Its quick onset and short duration make it suitable for dosing **immediately before meals** to control post-prandial glucose levels [1]. *Regular insulin* - **Regular insulin** is a **short-acting insulin**, with an onset of action around 30-60 minutes and a peak effect typically within 2-4 hours. - It is often administered **30 minutes before meals** and can also be used intravenously in acute situations like diabetic ketoacidosis. *Insulin glargine* - **Insulin glargine** is a **long-acting insulin** analog, providing a prolonged and relatively peakless effect over 24 hours [1, 2]. - Its primary role is to provide **basal insulin coverage**, mimicking the body's continuous background insulin production [1, 2].

Q: Which statin is considered most potent based on mg-to-mg LDL reduction capability?

Rosuvastatin. ***Rosuvastatin*** - **Rosuvastatin** is known for its high potency, achieving significant **LDL-C reduction** at relatively low doses. - It is often considered the most potent statin on a **milligram-to-milligram basis**. *Simvastatin* - **Simvastatin** is a moderate-intensity statin, not as potent as rosuvastatin or atorvastatin in reducing LDL-C. - While effective, it typically requires higher doses to achieve comparable **LDL-C reductions** seen with high-potency statins. *Pravastatin* - **Pravastatin** is a hydrophilic statin, generally considered to be of lower potency compared to other statins like rosuvastatin and atorvastatin. - It is often used in patients with **hepatic dysfunction** due to its different metabolic profile but offers less aggressive **LDL-C reduction**. *Atorvastatin* - **Atorvastatin** is a high-intensity statin, very effective in reducing LDL-C, and often used for aggressive lipid lowering. - While highly potent, **atorvastatin** is generally considered slightly less potent than **rosuvastatin** on a mg-to-mg basis, though both are used for high-intensity lipid therapy.

Q: What is a key difference between fosphenytoin and phenytoin?

Can be mixed with saline. **Can be mixed with saline** - **Fosphenytoin** is a water-soluble prodrug that is converted to phenytoin in the body; its solubility allows it to be **mixed with saline** solutions for intravenous administration, minimizing the risk of precipitation. - Unlike phenytoin, fosphenytoin's formulation avoids the need for propylene glycol, which is associated with adverse cardiovascular effects and makes phenytoin incompatible with saline. *Can be used in absence seizures* - Neither **fosphenytoin nor phenytoin** is effective for treating **absence seizures**, and they can sometimes worsen them. - **Ethosuximide** or **valproic acid** are the drugs of choice for absence seizures. *Can be given orally* - While **phenytoin** is commonly available in oral forms (capsules, chewable tablets, suspension), **fosphenytoin** is primarily designed for **parenteral administration** (intravenous or intramuscular). - Fosphenytoin is a prodrug that is rapidly converted to phenytoin *in vivo*, but it is not typically available or indicated for direct oral administration. *It is the drug of choice for myoclonic seizures* - Neither **fosphenytoin nor phenytoin** is the drug of choice for **myoclonic seizures**; they can exacerbate this type of seizure. - **Valproic acid** and **levetiracetam** are preferred treatments for myoclonic seizures due to their broader spectrum of activity.

Q: What is the mode of action of azathioprine?

T-cell blockade. ***T-cell blockade*** - Azathioprine is a **prodrug** that is metabolized into **6-mercaptopurine (6-MP)**, which then interferes with **purine synthesis** [1, 2]. - This interference inhibits the proliferation of **lymphocytes**, particularly **T-cells**, thereby blocking their immune response. *↑ IL-2* - An increase in **IL-2 (interleukin-2)** production would lead to enhanced T-cell proliferation and activity, which is the opposite effect of azathioprine. - **IL-2** is crucial for T-cell growth, differentiation, and survival, so drugs that increase it would boost, not suppress, the immune system. *Decreased lymphophagocytic activity* - This statement is not the primary mode of action of azathioprine. The drug's main effect is on the **synthesis of DNA and RNA** in rapidly dividing cells, including lymphocytes. - While immune suppression can indirectly affect various immune cell functions, the direct mechanism is not primarily a decrease in phagocytosis by lymphocytes. *Wide-spread antitumor activity* - Although 6-mercaptopurine, the active metabolite of azathioprine, is used in combination chemotherapy for some **hematological malignancies**, azathioprine itself is primarily known as an **immunosuppressant** in conditions like **autoimmune diseases** and **transplant rejection**. - Its antitumor activity is not typically described as "wide-spread," and its predominant use in pharmacology is for immune modulation.

Q: Which diuretic exhibits paradoxical antidiuretic activity in diabetes insipidus?

Thiazide diuretics. ***Thiazide diuretics*** - Thiazides cause a modest **volume depletion**, leading to increased proximal tubular reabsorption of water and solutes [1]. - They also lower the **glomerular filtration rate**, further reducing the amount of fluid delivered to the collecting ducts, thus paradoxically reducing urine output in diabetes insipidus [2]. - This effect is particularly useful in **nephrogenic diabetes insipidus**, where the kidneys cannot respond to ADH [2]. *Potassium-sparing diuretics (Triamterene)* - Triamterene is a **potassium-sparing diuretic** that blocks epithelial sodium channels in the late distal tubule and collecting duct. - It increases sodium and water excretion, which would worsen, not improve, the polyuria of diabetes insipidus. *Aldosterone antagonists (Spironolactone)* - Spironolactone is a **mineralocorticoid receptor antagonist** that increases sodium and water excretion while conserving potassium in the collecting duct. - Its primary action is to counteract aldosterone, and it does not exhibit the paradoxical antidiuretic effect seen with thiazides in diabetes insipidus. *Loop diuretics (Furosemide)* - Loop diuretics like furosemide act on the **thick ascending limb of the loop of Henle** to inhibit sodium, potassium, and chloride reabsorption. - They cause significant diuresis and would **exacerbate the polyuria** in patients with diabetes insipidus, rather than improving it.

Q: What is the recommended dosage for chloroquine chemoprophylaxis in malaria prevention?

500 mg once weekly. ***500 mg once weekly*** - The recommended dosage for chloroquine chemoprophylaxis in malaria prevention is **500 mg salt** (or equivalent to 300 mg base) administered **once weekly**. - This regimen ensures adequate blood concentrations to prevent malarial infection in endemic areas. *500 mg/week* - While the 500 mg dose is correct, simply stating "500 mg/week" without specifying "once weekly" could be misinterpreted. - Chloroquine is generally taken as a **single weekly dose**, not divided doses. *400 mg once weekly* - A dosage of **400 mg** is **sub-therapeutic** for weekly chloroquine chemoprophylaxis. - This dose would likely not provide sufficient protection against malaria. *500 mg BD/week* - Taking chloroquine **twice weekly (BD/week)** at 500 mg is excessive for chemoprophylaxis. - This regimen can lead to increased side effects and toxicity without providing additional prophylactic benefit.

Q: Which of the following drugs acts directly to induce an erection without the need for sexual stimulation?

Alprostadil. ***Alprostadil***- **Alprostadil** is a **prostaglandin E1** analog that can directly induce vasodilation in the penile arteries, leading to an erection without sexual stimulation [1].- It is typically administered via **intracavernosal injection** or as a **urethral suppository**.*Sildenafil*- **Sildenafil** is a **PDE5 inhibitor** that works by enhancing the effects of **nitric oxide**, which is released in response to sexual stimulation [2, 3].- It requires **sexual arousal** to be effective, as it doesn't directly initiate the erectile process [2, 3].*Tadalafil*- Similar to sildenafil, **tadalafil** is also a **PDE5 inhibitor** that works by increasing cGMP levels and promoting smooth muscle relaxation [2, 3].- Its action is dependent on the release of **nitric oxide** triggered by sexual stimulation [2, 3].*Testosterone*- **Testosterone** is a hormone involved in sex drive and overall erectile function over time, but it does not directly or acutely induce an erection.- Its primary role in erectile dysfunction is in cases of **hypogonadism**, and it requires sexual stimulation for its effects on erection.

Question 1

Romiplostim mimics which of the following receptors?

Accepted Answer

Thrombopoietin

Answer

IL 6

Answer

IL 8

Answer

PGE 1

Question 2

Sulphonamide injection causes decrease in folic acid by?

Accepted Answer

Inhibition through competition with substrate

Answer

Inhibition without competition

Answer

Inhibition through a different site

Answer

Inhibition that does not involve the active site

Question 3

Which of the following is the most common side effect of Cimetidine?

Accepted Answer

CNS effects (confusion, dizziness)

Answer

Diarrhea

Answer

Impotence

Answer

Gynaecomastia

Question 4

Which of the following is an intermediate-acting insulin?

Accepted Answer

NPH insulin

Answer

Insulin lispro

Answer

Insulin glargine

Answer

Regular insulin

Question 5

Which statin is considered most potent based on mg-to-mg LDL reduction capability?

Accepted Answer

Rosuvastatin

Answer

Simvastatin

Answer

Pravastatin

Answer

Atorvastatin

Question 6

What is a key difference between fosphenytoin and phenytoin?

Accepted Answer

Can be mixed with saline

Answer

Can be used in absence seizures

Answer

Can be given orally

Answer

It is the drug of choice for myoclonic seizures

Question 7

What is the mode of action of azathioprine?

Accepted Answer

T-cell blockade

Answer

↑ IL-2

Answer

Decreased lymphophagocytic activity

Answer

Wide-spread antitumor activity

Question 8

Which diuretic exhibits paradoxical antidiuretic activity in diabetes insipidus?

Accepted Answer

Thiazide diuretics

Answer

Aldosterone antagonists (Spironolactone)

Answer

Loop diuretics (Furosemide)

Answer

Potassium-sparing diuretics (Triamterene)

Question 9

What is the recommended dosage for chloroquine chemoprophylaxis in malaria prevention?

Accepted Answer

500 mg once weekly

Answer

500 mg/week

Answer

400 mg once weekly

Answer

500 mg BD/week

Question 10

Which of the following drugs acts directly to induce an erection without the need for sexual stimulation?

Accepted Answer

Alprostadil

Answer

Sildenafil

Answer

Tadalafil

Answer

Testosterone

NEET-PG 2012 — Pharmacology