Which of the following is a long-acting local anesthetic?
What is the progestogen of choice in emergency contraception?
What is the primary treatment indication of folic acid?
Which of the following drugs can lead to pemphigus?
Suxamethonium primarily acts on which type of receptors?
All of the following are medical uses of erythropoietin except?
Which vitamin/nutrient toxicity is associated with excessive sweating?
Which of the following medications is primarily used to decrease serum triglycerides?
Which of the following methods can reduce flushing caused by niacin?
Intracranial pressure may be increased by all of the following drugs except -
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 111: Which of the following is a long-acting local anesthetic?
- A. Dibucaine (Correct Answer)
- B. Prilocaine
- C. Procaine
- D. Lignocaine
Explanation: ***Dibucaine*** - **Dibucaine** is a **long-acting amide local anesthetic** with a duration of action up to 10 hours. - Its high **lipid solubility** contributes to its prolonged effect and greater potency compared to other local anesthetics. *Prilocaine* - **Prilocaine** is considered an **intermediate-duration amide local anesthetic**, with a duration of action typically 1-2 hours. - It carries a risk of **methemoglobinemia** at higher doses, which differentiates it from longer-acting agents. *Procaine* - **Procaine** is a **short-acting ester local anesthetic**, with a duration of action usually less than 1 hour. - It is known for its relatively **high allergenicity** due to its metabolism to para-aminobenzoic acid (PABA). *Lignocaine* - **Lignocaine (Lidocaine)** is an **intermediate-acting amide local anesthetic**, with a duration of action around 1-3 hours. - It is one of the most commonly used local anesthetics, but its duration is not as long as that of dibucaine.
Question 112: What is the progestogen of choice in emergency contraception?
- A. Norethisterone
- B. Medroxyprogesterone
- C. Oxytocin
- D. Levonorgestrel (Correct Answer)
Explanation: ***Correct Option: Levonorgestrel*** - **Levonorgestrel** is the **progestogen of choice** for **emergency contraception** (Plan B, morning-after pill) - It works by **inhibiting or delaying ovulation**, preventing fertilization - Also alters **cervical mucus** to prevent sperm penetration and may affect endometrial receptivity - WHO-recommended as **single dose (1.5 mg)** or two doses (0.75 mg each, 12 hours apart) - Most effective when taken **within 72 hours** of unprotected intercourse, preferably within 24 hours *Incorrect Option: Norethisterone* - **Norethisterone** is a progestogen used in **oral contraceptive pills** and for managing gynecological conditions (menorrhagia, endometriosis, dysmenorrhea) - While it has progestational effects, it is **not the first-line choice** for emergency contraception - Less effective than levonorgestrel for post-coital contraception *Incorrect Option: Medroxyprogesterone* - **Medroxyprogesterone acetate** is used as a **long-acting depot contraceptive** (Depo-Provera injection every 3 months) - Also used for hormone replacement therapy and treating endometrial hyperplasia - **Not suitable for emergency contraception** due to its formulation and mechanism of action *Incorrect Option: Oxytocin* - **Oxytocin** is a posterior pituitary hormone that causes **uterine contractions** during labor and **milk ejection** during breastfeeding - It has **no role in contraception** or preventing pregnancy - Used therapeutically for labor induction, postpartum hemorrhage prevention, and augmentation of labor
Question 113: What is the primary treatment indication of folic acid?
- A. Prevention of neural tube defects in pregnancy
- B. Treatment of megaloblastic anemia (Correct Answer)
- C. Management of hemoglobinopathies
- D. None of the above
Explanation: ***Treatment of megaloblastic anemia*** - Folic acid is essential for **DNA synthesis** and cell division, and its deficiency leads to impaired red blood cell maturation, causing **megaloblastic anemia**. - Supplementation with folic acid effectively reverses the hematological abnormalities in **folate-deficient megaloblastic anemia**. *Prevention of neural tube defects in pregnancy* - While folic acid is crucial for preventing **neural tube defects** (NTDs), this is a **prophylactic** rather than a primary therapeutic use. - The focus of this question is on the *primary therapeutic* use, implying treatment of an existing condition. *Management of hemoglobinopathies* - Hemoglobinopathies like **sickle cell anemia** or **thalassemia** are genetic disorders affecting hemoglobin structure or production, not primarily due to folic acid deficiency. - Folic acid may be given to these patients to support increased red blood cell turnover, but it does not address the underlying genetic defect. *None of the above* - This option is incorrect because folic acid has a clear primary therapeutic role in treating **megaloblastic anemia**.
Question 114: Which of the following drugs can lead to pemphigus?
- A. Carbamazepine
- B. Penicillamine (Correct Answer)
- C. Isoniazid
- D. Furosemide
Explanation: ***Penicillamine*** - **Penicillamine** is a well-known drug that can induce **pemphigus**, often through mechanisms involving alterations in **desmosome structure** or function. - The drug's sulfhydryl groups are thought to interfere with the integrity of **desmoglein proteins**, leading to blister formation. *Isoniazid* - **Isoniazid** is a first-line antituberculosis drug primarily associated with **hepatotoxicity** and **peripheral neuropathy**. - It is not typically implicated in the development of **pemphigus**. *Carbamazepine* - **Carbamazepine** is an anticonvulsant that can cause various cutaneous reactions, most notably **Stevens-Johnson syndrome (SJS)** and **toxic epidermal necrolysis (TEN)**. - While it can cause severe skin reactions, **pemphigus** is not a common side effect of carbamazepine. *Furosemide* - **Furosemide** is a loop diuretic that can cause **photosensitivity**, rashes, and rarely, severe skin reactions like **erythema multiforme**. - It is not recognized as a drug that induces **pemphigus**.
Question 115: Suxamethonium primarily acts on which type of receptors?
- A. Nicotinic acetylcholine receptors (Correct Answer)
- B. Potassium channels
- C. Calcium channels
- D. Chloride channels
Explanation: ***Nicotinic acetylcholine receptors*** - **Suxamethonium** is a depolarizing muscle relaxant that acts as an **agonist at nicotinic acetylcholine receptors** at the neuromuscular junction. - This initial activation leads to muscle fasciculations followed by prolonged depolarization, causing **flaccid paralysis**. *Potassium channels* - While some drugs may affect potassium channels to alter neuronal excitability, suxamethonium's primary mechanism of action is not on these channels. - Blocking potassium channels is characteristic of drugs like **certain antiarrhythmics** or **sulfonylureas**. *Calcium channels* - **Calcium channels** play a role in muscle contraction, but they are not the primary target of suxamethonium. - Drugs like **dihydropyridines** (e.g., nifedipine) target calcium channels for their antihypertensive effects. *Chloride channels* - Chloride channels are involved in maintaining resting membrane potential and inhibitory neurotransmission. - Drugs such as **benzodiazepines** indirectly enhance GABA-mediated chloride influx, which is distinct from suxamethonium's action.
Question 116: All of the following are medical uses of erythropoietin except?
- A. Treatment of anaemia associated with renal disease
- B. Chemotherapy induced anemia
- C. Megaloblastic Anemia (Correct Answer)
- D. Specific cases of anemia associated with Crohn's disease.
Explanation: ***Megaloblastic Anemia*** - Megaloblastic anemia is caused by **vitamin B12 or folate deficiency**, which impairs DNA synthesis and leads to the production of large, immature red blood cells. - Treatment involves supplementing the deficient vitamin (B12 or folate), as erythropoietin does not address the underlying cause of impaired red blood cell maturation. *Treatment of anaemia associated with renal disease* - **Erythropoietin** is primarily produced by the kidneys, and chronic kidney disease often leads to decreased erythropoietin production, resulting in anemia. - Administering exogenous erythropoietin stimulates red blood cell production, making it a critical treatment for **anemia of chronic kidney disease**. *Chemotherapy induced anemia* - Chemotherapy can suppress bone marrow function, leading to **decreased red blood cell production** and subsequent anemia. - Erythropoietin-stimulating agents can be used to mitigate this side effect by **stimulating erythropoiesis** in the bone marrow. *Specific cases of anemia associated with Crohn's disease.* - Anemia in Crohn's disease can have multiple causes, including iron deficiency from blood loss, malabsorption of vitamins, and **anemia of chronic disease**. - Erythropoietin may be considered in cases where the anemia is primarily due to **inflammation-induced suppression of erythropoiesis** or decreased erythropoietin response, particularly if other treatments are ineffective.
Question 117: Which vitamin/nutrient toxicity is associated with excessive sweating?
- A. Choline (Correct Answer)
- B. Biotin
- C. Folic acid
- D. Niacin (Vitamin B3)
Explanation: ***Choline*** - **Excessive sweating** is a recognized symptom of choline toxicity, often accompanied by a **fishy body odor**, hypotension, and gastrointestinal distress. - Choline plays a role in various metabolic pathways, and high doses can overwhelm these systems, leading to adverse effects. *Biotin* - **Biotin toxicity** is extremely rare, even at very high doses; there are no well-documented cases of adverse effects from excessive intake. - Symptoms like excessive sweating are not associated with biotin overdose. *Folic acid* - While high doses of **folic acid** can mask a **vitamin B12 deficiency**, side effects like gastrointestinal upset or sleep disturbances are rare. - Excessive sweating is **not a characteristic symptom** of folic acid toxicity. *Niacin (Vitamin B3)* - High doses of niacin, especially its nicotinic acid form, are well-known to cause **flushing, itching, and liver toxicity**. - While skin effects are common with niacin toxicity, **excessive sweating** as a primary symptom is not typically reported.
Question 118: Which of the following medications is primarily used to decrease serum triglycerides?
- A. Fibrates (Correct Answer)
- B. Ezetimibe
- C. Niacin
- D. Statin
Explanation: ***Fibrates*** - Fibrates, such as **gemfibrozil** and **fenofibrate**, are primarily used to activate **PPAR-alpha**, leading to increased lipoprotein lipase activity and reduced hepatic triglyceride synthesis. - This effectively lowers **serum triglyceride levels** by 20-50% and can also increase HDL cholesterol. *Statin* - Statins primarily inhibit **HMG-CoA reductase**, the rate-limiting enzyme in cholesterol synthesis, which makes them highly effective at lowering **LDL cholesterol**. - While they can cause a modest reduction in triglycerides (10-30%), this is not their primary mechanism or indication. *Ezetimibe* - Ezetimibe works by inhibiting the absorption of **cholesterol** at the brush border of the small intestine, thereby lowering **LDL cholesterol**. - It has minimal effect on **triglyceride levels** and is not indicated for primary triglyceride reduction. *Niacin* - Niacin, or **nicotinic acid**, reduces the liver's production of VLDL (which contains triglycerides) and LDL, and also increases HDL cholesterol. - While it can significantly lower triglycerides, its use is often limited by bothersome side effects such as **flushing** and itchiness, making fibrates generally preferred for primary triglyceride lowering due to better tolerability.
Question 119: Which of the following methods can reduce flushing caused by niacin?
- A. All of the options (Correct Answer)
- B. Tachyphylaxis
- C. Laropiprant
- D. Premedication with aspirin
Explanation: ***All of the options*** - **All three methods** (tachyphylaxis, laropiprant, and premedication with aspirin) are effective strategies for reducing niacin-induced flushing. - This demonstrates that multiple pharmacological and physiological approaches can mitigate this common side effect of niacin therapy. **Why each method works:** **Tachyphylaxis:** - Refers to the rapid decrease in response to a drug after repeated administration - With continued niacin use, tolerance develops and flushing intensity decreases over time - This is a natural adaptive response, though not an immediate solution for initial flushing episodes **Laropiprant:** - A selective antagonist of the **prostaglandin D2 receptor 1 (DP1)** - Specifically developed to reduce niacin-induced flushing by blocking prostaglandin D2-mediated vasodilation - Was marketed in combination with niacin (though later withdrawn due to other safety concerns) **Premedication with aspirin:** - **Aspirin** or other NSAIDs taken approximately 30 minutes before niacin administration - Reduces flushing by inhibiting **prostaglandin synthesis**, particularly prostaglandin D2 - Prostaglandins are key mediators of the cutaneous vasodilation that causes flushing
Question 120: Intracranial pressure may be increased by all of the following drugs except -
- A. Quinolones
- B. Aminoglycosides (Correct Answer)
- C. Vitamin A
- D. Corticosteroids
Explanation: ***Aminoglycosides*** - **Aminoglycosides** are not typically associated with increasing intracranial pressure. Their primary toxicities include **ototoxicity** and **nephrotoxicity**. - There is no established physiological mechanism by which aminoglycosides directly elevate ICP. *Vitamin A* - **Vitamin A toxicity**, particularly the chronic form of hypervitaminosis A, is a known cause of **idiopathic intracranial hypertension (pseudotumor cerebri)**, which directly increases ICP. - This occurs due to an unknown mechanism that leads to impaired CSF absorption or increased CSF production. *Corticosteroids* - While corticosteroids are often used to reduce cerebral edema and ICP, their **withdrawal**, particularly after prolonged use, can lead to rebound increases in ICP. - In certain susceptible individuals, or with paradoxical reactions, corticosteroids can also induce **pseudotumor cerebri**, leading to elevated ICP. *Quinolones* - **Quinolones** (fluoroquinolones) have been implicated in cases of **drug-induced intracranial hypertension (pseudotumor cerebri)**. - The mechanism is not fully understood but is thought to involve effects on **cerebrospinal fluid dynamics**.