Which vitamin/nutrient toxicity is associated with excessive sweating?
Which of the following medications is primarily used to decrease serum triglycerides?
All of the following are medical uses of erythropoietin except?
Which of the following is the only clinically available depolarizing muscle relaxant?
What is the treatment for extrapyramidal side effects induced by Haloperidol?
Which of the following drugs is an alpha 2 agonist?
Modafinil is primarily used for the treatment of which of the following conditions?
Which drug is not considered a mood stabilizer?
What is the mechanism of action of duloxetine?
Which of the following actions is NOT associated with tricyclic antidepressants?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 121: 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 122: 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 123: 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 124: Which of the following is the only clinically available depolarizing muscle relaxant?
- A. Decamethonium
- B. Suxamethonium (Correct Answer)
- C. Mivacurium
- D. None of the options
Explanation: ***Suxamethonium*** - **Suxamethonium** (also known as succinylcholine) is currently the **only depolarizing neuromuscular blocker** available for clinical use. - It works by mimicking acetylcholine, binding to and activating nicotinic acetylcholine receptors at the **neuromuscular junction**, causing initial muscle fasciculations followed by relaxation. *Decamethonium* - **Decamethonium** is a depolarizing neuromuscular blocker but is **no longer clinically available** due to its prolonged action and side effects. - It also acts by opening nicotinic acetylcholine receptor channels, leading to depolarization and muscle paralysis. *Mivacurium* - **Mivacurium** is a **nondepolarizing neuromuscular blocker**, meaning it acts as a competitive antagonist at the acetylcholine receptor. - It is known for its **short duration of action** due to rapid hydrolysis by plasma cholinesterases but is not depolarizing. *None of the options* - This option is incorrect because suxamethonium is indeed a clinically available depolarizing muscle relaxant. - The question specifically asks for the *only* clinically available one, which suxamethonium fulfills.
Question 125: What is the treatment for extrapyramidal side effects induced by Haloperidol?
- A. Barbiturates
- B. SSRIs
- C. Benzodiazepines
- D. Anticholinergic drugs (Correct Answer)
Explanation: ***Anticholinergic drugs (effective treatment)*** - **Anticholinergic medications**, such as **benztropine** or **diphenhydramine**, are the primary treatment for **acute extrapyramidal symptoms (EPS)** like dystonia and parkinsonism induced by antipsychotics like haloperidol. - They work by **blocking muscarinic acetylcholine receptors**, helping to restore the balance between dopamine and acetylcholine in the basal ganglia. *Benzodiazepines (used for anxiety and muscle relaxation)* - While benzodiazepines can offer some relief for **akathisia** (a form of EPS characterized by restlessness) due to their sedative and muscle relaxant properties, they are **not the first-line treatment for other acute EPS** such as dystonia or parkinsonism. - They primarily enhance **GABAergic transmission** and are effective for anxiety and seizure control rather than direct antagonism of EPS mechanisms. *Barbiturates (used as sedative-hypnotic drugs)* - **Barbiturates** are strong central nervous system depressants used for sedation, anesthesia, and seizure control, but are **not indicated for the treatment of EPS**. - Their significant **sedative and addictive potential**, along with a narrow therapeutic index, makes them unsuitable for this purpose. *SSRIs (used for depression and anxiety)* - **SSRIs (Selective Serotonin Reuptake Inhibitors)** are antidepressants that work by increasing serotonin levels in the brain and are used to treat depression, anxiety, and obsessive-compulsive disorder. - They **do not have a direct role** in ameliorating dopamine-acetylcholine imbalance responsible for haloperidol-induced EPS.
Question 126: Which of the following drugs is an alpha 2 agonist?
- A. Apraclonidine (Correct Answer)
- B. Timolol
- C. PG analogues
- D. Verapamil
Explanation: ***Apraclonidine*** - **Apraclonidine** is a synthetic **alpha-2 adrenergic agonist** that reduces aqueous humor production and increases uveoscleral outflow, thereby lowering intraocular pressure. - It is primarily used for the short-term treatment of **open-angle glaucoma** or ocular hypertension. *Timolol* - **Timolol** is a **non-selective beta-adrenergic blocker** that reduces aqueous humor production, leading to a decrease in intraocular pressure. - It does not act on alpha-2 receptors, distinguishing it from apraclonidine. *PG analogues* - **Prostaglandin analogues** (PG analogues) such as latanoprost, bimatoprost, and travoprost are primarily used to treat glaucoma by **increasing uveoscleral outflow** of aqueous humor. - They act on **prostaglandin F2α receptors**, not alpha-2 adrenergic receptors. *Verapamil* - **Verapamil** is a **calcium channel blocker** primarily used to treat hypertension, angina, and arrhythmias. - It acts by blocking calcium channels in vascular smooth muscle and the heart, and does not have significant alpha-2 adrenergic agonist activity.
Question 127: Modafinil is primarily used for the treatment of which of the following conditions?
- A. Narcolepsy (Correct Answer)
- B. Sexual dysfunction
- C. Depression
- D. Anxiety
Explanation: ***Narcolepsy*** - **Modafinil** is a **eugeroic** (wakefulness-promoting agent) specifically approved and widely used for the treatment of excessive daytime sleepiness associated with **narcolepsy**. - Its mechanism involves increasing **dopamine** and **norepinephrine** levels, and modulating **orexin** pathways, promoting alertness without significant psychomotor stimulation. *Sexual dysfunction* - While sometimes explored off-label for certain types of sexual dysfunction, **modafinil** is not a primary or approved treatment for this condition. - Primary treatments for sexual dysfunction often involve specific medications like **PDE5 inhibitors** or hormone therapy, depending on the cause. *Depression* - **Modafinil** is not a primary antidepressant, although it can be used as an **adjunctive therapy** in some cases to combat residual fatigue or hypersomnia associated with depression. - Standard treatment for depression involves **selective serotonin reuptake inhibitors (SSRIs)**, **serotonin-norepinephrine reuptake inhibitors (SNRIs)**, or other classes of antidepressants. *Anxiety* - **Modafinil** is a stimulant-like drug and can sometimes **exacerbate anxiety** in susceptible individuals due to its catecholaminergic effects. - Primary treatments for anxiety disorders include **selective serotonin reuptake inhibitors (SSRIs)**, **benzodiazepines** (for acute relief), and psychotherapy.
Question 128: Which drug is not considered a mood stabilizer?
- A. Lithium
- B. Lamotrigine
- C. Imipramine (Correct Answer)
- D. Carbamazepine
Explanation: ***Imipramine*** - Imipramine is a **tricyclic antidepressant (TCA)**, primarily used to treat depression, not to stabilize mood in bipolar disorder. - TCAs can sometimes induce **mania** or hypomania in individuals with bipolar disorder, thus they are generally not used as monotherapy for mood stabilization. *Lithium* - **Lithium** is considered the gold standard and one of the oldest and most effective **mood stabilizers** for bipolar disorder. - It works by modulating **neurotransmitter systems** and second messenger pathways in the brain. *Lamotrigine* - **Lamotrigine** is an **anticonvulsant** medication that is also recognized as an effective **mood stabilizer**, particularly for preventing depressive episodes in bipolar disorder. - Its mechanism involves stabilizing neuronal membranes by blocking **voltage-gated sodium channels**. *Carbamazepine* - **Carbamazepine** is an **anticonvulsant** medication often used as a **mood stabilizer** for the treatment of acute manic and mixed episodes in bipolar disorder. - It works by reducing the excitability of nerve impulses through blocking **voltage-sensitive sodium channels**.
Question 129: What is the mechanism of action of duloxetine?
- A. Selective serotonin reuptake inhibition
- B. Selective norepinephrine reuptake inhibition
- C. Inhibition of both serotonin and norepinephrine reuptake (Correct Answer)
- D. No effect on neurotransmitter reuptake
Explanation: ***Inhibition of both serotonin and norepinephrine reuptake*** - **Duloxetine** is a **serotonin-norepinephrine reuptake inhibitor (SNRI)**, meaning it blocks the reuptake of both neurotransmitters, increasing their concentrations in the synaptic cleft [2]. - This dual action contributes to its efficacy in treating **depression**, **anxiety disorders**, and **neuropathic pain** [2], [3]. *Selective serotonin reuptake inhibition* - This describes the mechanism of **SSRIs (Selective Serotonin Reuptake Inhibitors)**, such as fluoxetine or sertraline, which primarily target serotonin [1]. - Duloxetine's mechanism is broader, affecting both serotonin and norepinephrine [2]. *Selective norepinephrine reuptake inhibition* - This mechanism is characteristic of medications like **atomoxetine**, used for ADHD, which primarily targets norepinephrine. - Duloxetine has a dual action, not selective to norepinephrine alone. *No effect on neurotransmitter reuptake* - Medications with no effect on neurotransmitter reuptake would not typically be effective as antidepressants or treatments for neuropathic pain. - Duloxetine's therapeutic effects are directly linked to its inhibition of reuptake for both serotonin and norepinephrine [2], [4].
Question 130: Which of the following actions is NOT associated with tricyclic antidepressants?
- A. Block 5-HT or NE reuptake
- B. Anticholinergic action
- C. MAO inhibition (Correct Answer)
- D. Causes sedation
Explanation: ***MAO inhibition*** - Tricyclic antidepressants (TCAs) primarily exert their effects by inhibiting the reuptake of **norepinephrine** and **serotonin**, not by inhibiting monoamine oxidase (MAO). - **MAO inhibitors** are a distinct class of antidepressants with a different mechanism of action and side effect profile. *Anticholinergic action* - Many TCAs have significant **anticholinergic effects**, blocking muscarinic receptors and leading to side effects like dry mouth, constipation, and blurred vision. - These effects contribute to the **adverse event profile** of TCAs, especially in elderly patients. *Block 5-HT or NE reuptake* - The primary mechanism of action of TCAs involves the **inhibition of serotonin (5-HT)** and **norepinephrine (NE) reuptake** into presynaptic neurons. - This action increases the concentration of these neurotransmitters in the **synaptic cleft**, thereby potentiating their effects. *Causes sedation* - TCAs frequently cause **sedation**, particularly the more histaminergic ones (e.g., amitriptyline, doxepin), due to their **histamine H1 receptor antagonism**. - This side effect can be beneficial for patients with insomnia but can be problematic for daytime functioning.