NEET-PG 2015 - Pharmacology Practice Questions

Q: Hyoscine is an antagonist at which cholinergic receptor?

Muscarinic. ***Muscarinic*** - **Hyoscine** (scopolamine) is a well-known **antagonist** at **muscarinic cholinergic receptors**. - It blocks the action of **acetylcholine** at these receptors, leading to its anticholinergic effects like treating motion sickness and reducing secretions. *Nicotinic* - **Hyoscine** does not primarily act on **nicotinic cholinergic receptors**. - Drugs acting on nicotinic receptors include **neuromuscular blockers** (e.g., succinylcholine, rocuronium) and **ganglionic blockers**, which have different clinical applications. *Both* - While some drugs may have activity at both receptor types, **hyoscine's primary and clinically significant antagonism is at muscarinic receptors**. - Its therapeutic effects are attributed almost exclusively to its **muscarinic blockade**. *None of the above* - This option is incorrect because **hyoscine is a clear antagonist at muscarinic cholinergic receptors**. - Its widespread use in medicine is based on this specific pharmacological action.

Q: Fenoldopam is used in the management of?

Hypertensive emergencies. ***Hypertensive emergencies*** - **Fenoldopam** is a **dopamine D1 receptor agonist** that causes rapid, dose-dependent peripheral vasodilation and increased renal blood flow, making it suitable for acute blood pressure reduction during hypertensive emergencies. - Its **rapid onset** and short half-life allow for precise control of blood pressure, and its **benefit** in preserving or improving renal function is particularly beneficial in patients with renal impairment. *Congestive heart failure* - While fenoldopam can increase renal blood flow, it is not a primary treatment for **congestive heart failure (CHF)** and is not typically used for its management. - Other drug classes, such as **diuretics**, **ACE inhibitors**, and **beta-blockers**, are the mainstays of CHF treatment. *Migraine prophylaxis* - Fenoldopam has **no role** in the prevention or acute treatment of migraines. - **Beta-blockers**, **calcium channel blockers**, and certain **antidepressants** are commonly used for migraine prophylaxis. *Tachyarrhythmias* - Fenoldopam **does not have antiarrhythmic properties** and is not indicated for the treatment of tachyarrhythmias. - **Beta-blockers**, **calcium channel blockers**, and specific **antiarrhythmic drugs** are used to manage tachyarrhythmias.

Q: Which of the following is not a known side effect of amiodarone?

Hyperglycemia. ***Hyperglycemia*** - **Hyperglycemia** is generally **not recognized** as a direct or common side effect of amiodarone. - Amiodarone's primary action is on cardiac ion channels, and its metabolic effects typically involve thyroid function, not glucose regulation. *Hyperthyroidism* - Amiodarone contains **iodine**, which can induce **thyroid dysfunction**, including both hypo- and hyperthyroidism. - **Amiodarone-induced hyperthyroidism (AIH)** can occur due to increased thyroid hormone synthesis or destructive thyroiditis. *Peripheral neuropathy* - **Neurological side effects**, including **peripheral neuropathy**, are known to occur with chronic amiodarone use. - Symptoms often include **paresthesias**, weakness, and sensory loss in the extremities. *Skin discoloration* - Prolonged use of amiodarone can lead to **bluish-gray skin discoloration**, particularly in sun-exposed areas. - This is due to the **accumulation of amiodarone** and its metabolites in the skin.

Q: Which class of antihypertensive drugs is known to cause erectile dysfunction?

Beta-blockers. ***Beta-blockers*** - **Beta-blockers** are the antihypertensive class most commonly associated with **erectile dysfunction** - Mechanism: Reduced cardiac output, decreased peripheral blood flow, central nervous system effects reducing libido, and blockade of β2-mediated vasodilation - **Non-selective beta-blockers** (propranolol, nadolol) have higher incidence of ED compared to selective β1-blockers (metoprolol, atenolol) - Newer vasodilating beta-blockers (nebivolol, carvedilol) have lower risk of sexual dysfunction *Calcium channel blockers* - Generally have **neutral or minimal effect** on erectile function - May even improve ED in some patients due to **vasodilatory properties** - Side effects include peripheral edema and headache, but not sexual dysfunction *ACE inhibitors* - Associated with **lower risk of erectile dysfunction** compared to other antihypertensives - May have neutral or even protective effects on sexual function - Preferred choice for hypertensive patients with existing sexual dysfunction concerns - Common side effects: dry cough and angioedema (not related to sexual function) *AT1 receptor antagonists* - **ARBs have neutral to potentially beneficial effects** on sexual function - Considered an excellent alternative for patients experiencing sexual side effects with other antihypertensive medications - Some studies suggest they may improve erectile function in hypertensive patients

Q: How do thiazides cause hypercalcemia?

Decreased calcium excretion. ***Decreased calcium excretion*** - Thiazides inhibit the **Na-Cl co-transporter** in the **distal convoluted tubule**, leading to increased reabsorption of calcium [1], [2]. - This increased reabsorption of calcium is mediated by a low intracellular sodium concentration, which enhances the activity of the **Na+/Ca2+ exchanger** on the basolateral membrane [1]. *Increased parathyroid hormone secretion* - Thiazides **do not directly stimulate** parathyroid hormone (PTH) secretion; instead, they *decrease* calcium excretion, which would typically *lower* PTH levels through negative feedback. - Elevated PTH would lead to increased bone resorption and kidney calcium reabsorption, but this is not the **primary mechanism** for thiazide-induced hypercalcemia [2]. *Decreased calcitonin secretion* - **Calcitonin** is a hormone that *lowers* blood calcium levels, and its decrease would theoretically contribute to hypercalcemia. - However, thiazides have **no direct effect** on calcitonin secretion, making this an unlikely primary mechanism. *Increased calcium absorption* - While increased calcium absorption from the gut can contribute to hypercalcemia, thiazides do **not directly increase intestinal calcium absorption**. - Their primary action for influencing calcium levels is within the **kidney**, specifically on reabsorption, not absorption from the GI tract [1], [2].

Q: Which diuretic is most likely to cause hyponatremia by impairing free water excretion?

Thiazide diuretics. ***Thiazide diuretics*** - **Thiazide diuretics** inhibit the **Na-Cl cotransporter in the distal convoluted tubule (DCT)**, impairing the kidney's ability to dilute urine and excrete free water - This impaired urinary dilution leads to **water retention relative to sodium**, resulting in **dilutional hyponatremia** - **Most common in elderly patients**, those on low-salt diets, or with pre-existing volume depletion - **Mechanism**: By blocking sodium reabsorption in the DCT (a key site for urinary dilution), thiazides prevent the generation of free water, leading to hyponatremia when water intake continues *Loop diuretics* - **Loop diuretics** inhibit the **Na-K-2Cl cotransporter in the thick ascending limb of Henle**, causing significant diuresis - They impair the medullary concentration gradient, **enhancing free water excretion** - **Less likely to cause hyponatremia** compared to thiazides because they promote rather than impair free water clearance - When hyponatremia occurs with loop diuretics, it's usually due to concurrent SIADH or excessive free water intake *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** acting primarily on the **proximal tubule** - Causes **bicarbonate and sodium excretion**, leading to mild diuresis - Main side effect is **metabolic acidosis** (type 2 RTA) - **Does not significantly impair free water excretion**, making hyponatremia uncommon *Amiloride* - **Amiloride** is a **potassium-sparing diuretic** that blocks **epithelial sodium channels (ENaC) in the collecting duct** - Weak diuretic effect, primarily used to prevent potassium loss - **Does not impair urinary dilution mechanisms**, so hyponatremia is rare - Main concern is **hyperkalemia**, especially with ACE inhibitors or in renal insufficiency

Q: Which ACE inhibitor is safe in renal failure?

Benazepril. ***Benazepril*** - Among the listed ACE inhibitors, benazepril has the **most favorable excretion profile** in renal failure with approximately **50% renal and 50% hepatic elimination** (dual excretion pathway). - This balanced elimination reduces the risk of drug accumulation compared to predominantly renally excreted ACE inhibitors. - While dose adjustment may still be needed in **severe renal impairment**, benazepril is considered the **safest option among those listed** for patients with renal dysfunction. - **Note:** Fosinopril (not listed here) has true 50/50 dual elimination and requires no dose adjustment in renal failure, making it the ideal choice in clinical practice. *Captopril* - This ACE inhibitor undergoes predominantly **renal excretion (95%)** as unchanged drug and metabolites. - Requires significant **dose reduction** in renal failure to prevent accumulation and adverse effects including **hyperkalemia** and **hypotension**. - Less safe than benazepril in renal impairment due to heavy dependence on renal elimination. *Enalapril* - Enalapril is a prodrug converted to **enalaprilat**, with approximately **90% renal excretion**. - Dose adjustment is mandatory based on **creatinine clearance** in patients with renal failure. - Higher risk of accumulation and toxicity compared to dual-elimination ACE inhibitors like benazepril.

Q: Which sympathomimetic drug is primarily known to increase heart rate?

Isoprenaline. ***Isoprenaline*** - **Isoprenaline** (isoproterenol) is a non-selective beta-adrenergic agonist, with a strong affinity for **β1 and β2 receptors** [1]. - Its activation of **β1 receptors** in the heart leads to a significant increase in **heart rate (positive chronotropy)** and contractility (positive inotropy) [1]. - It is the **most potent chronotropic agent** among sympathomimetics and is primarily known for increasing heart rate [2]. *Phenylephrine* - **Phenylephrine** is a selective **α1 adrenergic agonist** that causes vasoconstriction [4]. - It increases blood pressure but typically causes **reflex bradycardia** (decreased heart rate) due to baroreceptor activation. - Does NOT directly increase heart rate. *Noradrenaline* - **Noradrenaline** (norepinephrine) primarily acts on **α1 receptors** causing vasoconstriction, and to a lesser extent on **β1 receptors** [3]. - While it can stimulate β1 receptors, its predominant effect is to increase **mean arterial pressure** through vasoconstriction, often causing **reflex bradycardia** [3]. *Adrenaline* - **Adrenaline** (epinephrine) acts on **α1, β1, and β2 receptors** [4]. While it does increase heart rate via **β1 receptor** stimulation, it also causes significant **vasoconstriction** (via α1) and **vasodilation** (via β2). - Its cardiovascular effects are more complex and dose-dependent compared to isoprenaline's specific chronotropic action.

Q: Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:

ACE inhibitors. ***ACE inhibitors*** - Spironolactone is a **potassium-sparing diuretic** that increases potassium levels by blocking aldosterone's effects in the collecting duct [1]. - **ACE inhibitors** also decrease aldosterone production [2], leading to reduced potassium excretion and a significant risk of **severe hyperkalemia** when combined with spironolactone [1, 2].*Beta-blockers* - While beta-blockers can cause a slight increase in plasma potassium by inhibiting cellular potassium uptake, this effect is generally modest and does not pose a major hyperkalemia risk when co-administered with spironolactone. - Their primary interaction concerns blood pressure and heart rate, not direct potassium handling.*Amlodipine* - Amlodipine is a **calcium channel blocker** that primarily causes vasodilation and does not significantly alter potassium balance. - Therefore, it does not substantially increase the risk of hyperkalemia when used concurrently with spironolactone.*Chlorothiazide* - Chlorothiazide is a **thiazide diuretic** that promotes potassium excretion, leading to a risk of hypokalemia. - When combined with spironolactone, a potassium-sparing diuretic, these agents can **partially offset each other's effects** on potassium balance, potentially reducing the risk of hyperkalemia compared to ACE inhibitors.

Q: At which receptor is the primary action of antipsychotic medications required?

D2 dopaminergic. ***D2 dopaminergic*** - The **antipsychotic effects** of typical (first-generation) antipsychotics are primarily mediated through **D2 receptor blockade** [1]. - Blocking D2 receptors in the **mesolimbic pathway** helps reduce positive symptoms of psychosis like hallucinations and delusions [2]. *M, muscarinic* - **Muscarinic receptor blockade** is a common adverse effect of some antipsychotics, leading to anticholinergic side effects such as **dry mouth** and **blurred vision**, rather than their primary therapeutic action. - This action does not directly contribute to the antipsychotic effect. *D1 dopaminergic* - While D1 receptors are involved in dopamine signaling, they are **not the primary target** for the antipsychotic action of most drugs [1]. - Some atypical antipsychotics may affect D1 receptors, but it's secondary to their D2 antagonism and serotonin modulation. *5HT4 serotonergic* - **Serotonin receptors (5HT)**, particularly 5HT2A, are important targets for atypical (second-generation) antipsychotics. - However, 5HT4 receptors are **not a primary target** for the antipsychotic effects, and 5HT2A blockade modulates dopamine release, which is still connected to the D2 hypothesis.

Question 1

Hyoscine is an antagonist at which cholinergic receptor?

Accepted Answer

Muscarinic

Answer

Nicotinic

Answer

Both

Answer

None of the above

Question 2

Fenoldopam is used in the management of?

Accepted Answer

Hypertensive emergencies

Answer

Congestive heart failure

Answer

Migraine prophylaxis

Answer

Tachyarrhythmias

Question 3

Which of the following is not a known side effect of amiodarone?

Accepted Answer

Hyperglycemia

Answer

Peripheral neuropathy

Answer

Hyperthyroidism

Answer

Skin discoloration

Question 4

Which class of antihypertensive drugs is known to cause erectile dysfunction?

Accepted Answer

Beta-blockers

Answer

Calcium channel blocker

Answer

ACE inhibitors

Answer

AT1 receptor antagonists

Question 5

How do thiazides cause hypercalcemia?

Accepted Answer

Decreased calcium excretion

Answer

Increased parathyroid hormone secretion

Answer

Decreased calcitonin secretion

Answer

Increased calcium absorption

Question 6

Which diuretic is most likely to cause hyponatremia by impairing free water excretion?

Accepted Answer

Thiazide diuretics

Answer

Loop diuretics

Answer

Acetazolamide

Answer

Amiloride

Question 7

Which ACE inhibitor is safe in renal failure?

Accepted Answer

Benazepril

Answer

Captopril

Answer

Enalapril

Answer

None of the options

Question 8

Which sympathomimetic drug is primarily known to increase heart rate?

Accepted Answer

Isoprenaline

Answer

Phenylephrine

Answer

Noradrenaline

Answer

Adrenaline

Question 9

Which of the following agents requires the MOST caution when combined with spironolactone due to increased risk of hyperkalemia:

Accepted Answer

ACE inhibitors

Answer

Beta-blockers

Answer

Amlodipine

Answer

Chlorothiazide

Question 10

At which receptor is the primary action of antipsychotic medications required?

Accepted Answer

D2 dopaminergic

Answer

M, muscarinic

Answer

5HT4 serotonergic

Answer

D1 dopaminergic

NEET-PG 2015 — Pharmacology