Which of the following methods can reduce flushing caused by niacin?
Which of the following metal ions is associated with secondary Parkinsonisms?
What is the drug of choice (DOC) for the treatment of subacute sclerosing panencephalitis (SSPE)?
Which vitamin/nutrient toxicity is associated with excessive sweating?
Which of the following medications is primarily used to decrease serum triglycerides?
Intracranial pressure may be increased by all of the following drugs except -
A patient undergoing a minor surgical procedure is given lignocaine injection. Assertion: Local anaesthetics act by blocking nerve conduction. Reason: Small fibers and non-myelinated fibers are blocked more easily than large myelinated fibers.
All of the following are medical uses of erythropoietin except?
What is the progestogen of choice in emergency contraception?
What is the primary treatment indication of folic acid?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 111: 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flushing by blocking prostaglandin D2-mediated vasodilation - Was marketed in combination with niacin (though later withdrawn due to other safety concerns) **Premedication with aspirin:** - **Aspirin** or other NSAIDs taken approximately 30 minutes before niacin administration -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 112: Which of the following metal ions is associated with secondary Parkinsonisms?
- A. Magnesium (Mg)
- B. Selenium (Se)
- C. Manganese (Mn) (Correct Answer)
- D. Molybdenum (Mo)
Explanation: ***Manganese (Mn)*** - Chronic exposure to high levels of **manganese** can lead to **manganism**, a neurological disorder characterized by **Parkinsonian-like symptoms**, including bradykinesia, rigidity, and gait disturbances [1]. - This is due to manganese accumulation in the **basal ganglia**, particularly the **globus pallidus**, affecting dopaminergic pathways. *Magnesium (Mg)* - **Magnesium** is an essential mineral vital for numerous bodily functions, including nerve and muscle function. - While imbalances can cause neurological issues (e.g., tremors with hypomagnesemia), it is not directly associated with **secondary parkinsonism**. *Selenium (Se)* - **Selenium** is a trace element with antioxidant properties, important for thyroid hormone metabolism and immune function. - Both deficiency and toxicity can cause various health problems, but it is not known to cause **secondary parkinsonism**. *Molybdenum (Mo)* - **Molybdenum** is an essential trace element that functions as a cofactor for several enzymes. - No known association exists between molybdenum exposure, deficiency, or toxicity and the development of **secondary parkinsonism**.
Question 113: What is the drug of choice (DOC) for the treatment of subacute sclerosing panencephalitis (SSPE)?
- A. Abacavir
- B. Inosine pranobex (Correct Answer)
- C. Glatiramer
- D. Interferon
Explanation: ***Inosine pranobex*** - **Inosine pranobex (Isoprinosine)** is considered the **oral drug of choice** for treating **subacute sclerosing panencephalitis (SSPE)**, particularly in the early stages, as it has shown success in delaying disease progression. - This drug works by **modulating the immune system** and enhancing T-cell function, which helps control the persistent measles virus infection in the CNS. - **Note:** Best outcomes are achieved when inosine pranobex is combined with **intrathecal/intraventricular interferon-alpha**, but as a single oral agent, inosine pranobex is the primary choice. *Abacavir* - **Abacavir** is an **antiretroviral drug (NRTI)** used in the treatment of **HIV infection**. - It inhibits reverse transcriptase and has **no role** in treating measles virus-induced SSPE. *Glatiramer* - **Glatiramer acetate** is an **immunomodulatory drug** used in **multiple sclerosis (MS)**. - It works by mimicking **myelin basic protein** to reduce immune attacks on myelin, but is **not effective** against viral infections like SSPE. *Interferon* - **Interferon-alpha** (particularly **intrathecal/intraventricular** administration) has been used in **SSPE** as **combination therapy** with inosine pranobex, showing improved outcomes. - However, when given systemically alone, it has **significant side effects** and **variable efficacy**. - As a single answer option without specifying the route, **inosine pranobex** is preferred as the primary oral DOC.
Question 114: 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 115: 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 116: 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**.
Question 117: A patient undergoing a minor surgical procedure is given lignocaine injection. Assertion: Local anaesthetics act by blocking nerve conduction. Reason: Small fibers and non-myelinated fibers are blocked more easily than large myelinated fibers.
- A. Assertion is false, but Reason is true
- B. Both Assertion and Reason are true, and Reason is not the correct explanation for Assertion (Correct Answer)
- C. Both Assertion and Reason are true, and Reason is the correct explanation for Assertion
- D. Assertion is true, but Reason is false
Explanation: ***Both Assertion and Reason are true, and Reason is NOT the correct explanation for Assertion*** - The **Assertion** is true: Local anesthetics (like lignocaine) block nerve conduction by inhibiting **voltage-gated sodium channels**, preventing the depolarization necessary for action potential propagation - The **Reason** is also true: Small diameter and non-myelinated fibers (like C and Aδ pain fibers) are blocked more easily than large myelinated fibers (like Aα motor fibers), which explains the **differential blockade** pattern seen clinically - However, the **Reason does NOT explain WHY** local anesthetics block nerve conduction—it describes **WHICH** nerve fibers are blocked preferentially. The mechanism of blocking conduction is sodium channel inhibition, not fiber size selectivity - The differential sensitivity is a consequence of fiber characteristics (surface area-to-volume ratio, number of nodes of Ranvier), not the explanation for the blocking mechanism itself *Both Assertion and Reason are true, and Reason is the correct explanation for Assertion* - While both statements are individually true, the Reason does not explain the **mechanism** by which local anesthetics block nerve conduction - The Reason addresses fiber **selectivity**, which is a separate pharmacological property from the **mechanism of action** (sodium channel blockade) *Assertion is true, but Reason is false* - The Assertion is demonstrably true—local anesthetics block nerve conduction - The Reason is also true—this is well-established pharmacology: autonomic (small) > sensory (medium) > motor (large) fiber blockade sequence *Assertion is false, but Reason is true* - The Assertion is fundamentally correct and represents the primary pharmacological action of local anesthetics - Blocking nerve conduction is the therapeutic goal of local anesthetic administration
Question 118: 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 119: 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 120: 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**.