Autonomic Nervous System Drugs Practice Questions

Q: Which skeletal muscle relaxant causes significant release of histamine?

D-tubocurarine. ### Explanation **Correct Option: D. D-tubocurarine** D-tubocurarine is a prototype non-depolarizing neuromuscular blocker (benzylisoquinoline class). It is notorious for causing **significant histamine release** from mast cells. This occurs through a direct non-immunologic mechanism. The systemic release of histamine leads to clinical manifestations such as **hypotension, bronchospasm, flushing, and excessive salivary/bronchial secretions**. Due to these side effects and the availability of safer alternatives, its clinical use is now obsolete. **Analysis of Incorrect Options:** * **A. Pancuronium:** An aminosteroid muscle relaxant. It does not cause histamine release but is known for its **vagolytic effect**, which causes tachycardia and hypertension. * **B. Atracurium:** While it can cause some histamine release (especially at high doses), it is significantly less potent in this regard than D-tubocurarine. Its primary clinical highlight is metabolism via **Hofmann elimination**, making it safe in liver and kidney failure. * **C. Gallamine:** An older synthetic agent that lacks significant histamine-releasing properties but, like pancuronium, has strong antimuscarinic (vagolytic) effects leading to tachycardia. **High-Yield Clinical Pearls for NEET-PG:** * **Histamine Releasers:** D-tubocurarine (Maximum) > Atracurium > Mivacurium. * **Safest in Renal/Hepatic Failure:** Atracurium and Cisatracurium (due to Hofmann elimination). * **Drug of Choice for Rapid Sequence Induction:** Succinylcholine (fastest onset, shortest duration). * **Vagolytic Agents:** Pancuronium and Gallamine (cause tachycardia). * **Cisatracurium:** An isomer of atracurium that is more potent and produces **negligible histamine release**, making it the preferred benzylisoquinoline in clinical practice.

Q: Reflex tachycardia is most likely to occur after the systemic administration of which of the following drugs?

albuterol. **Explanation:** The correct answer is **albuterol**. This question tests your understanding of the baroreceptor reflex and the vascular effects of adrenergic agonists. **1. Why Albuterol is Correct:** Albuterol is a selective **$\beta_2$-adrenergic agonist**. While primarily used for bronchodilation, systemic administration causes stimulation of $\beta_2$ receptors in the peripheral vasculature, leading to **vasodilation** and a decrease in peripheral vascular resistance (PVR). This drop in blood pressure triggers the **baroreceptor reflex**, resulting in a compensatory increase in sympathetic outflow to the heart (reflex tachycardia). Additionally, at higher doses, albuterol may lose selectivity and directly stimulate $\beta_1$ receptors in the heart, further increasing the heart rate. **2. Why the Other Options are Incorrect:** * **Methoxamine & Phenylephrine:** Both are selective **$\alpha_1$-adrenergic agonists**. They cause potent vasoconstriction, which increases peripheral vascular resistance and blood pressure. This rise in pressure triggers the baroreceptor reflex to increase vagal (parasympathetic) tone, leading to **reflex bradycardia**, not tachycardia. * **Propranolol:** This is a non-selective **$\beta$-blocker**. It blocks $\beta_1$ receptors in the heart, directly causing a decrease in heart rate (**bradycardia**). It would actually inhibit a reflex tachycardic response. **Clinical Pearls for NEET-PG:** * **Rule of Thumb:** Drugs that cause significant vasodilation (e.g., Hydralazine, Nitrates, $\alpha$-blockers, $\beta_2$-agonists) typically cause reflex tachycardia. * **Vasoconstrictors** that increase mean arterial pressure (e.g., Phenylephrine, Norepinephrine) typically cause reflex bradycardia. * **Isoproterenol** ($\beta_1 + \beta_2$) causes the most profound tachycardia because it combines direct cardiac stimulation ($\beta_1$) with reflex tachycardia due to vasodilation ($\beta_2$).

Q: Which of the following is an alpha-1 blocker?

Tamsulosin. **Explanation:** The question asks for an alpha-1 blocker, and while options A, B, and C are all technically alpha-1 antagonists, **Tamsulosin** is the most specific answer in many clinical contexts due to its subtype selectivity. **1. Why Tamsulosin is the Correct Answer:** Tamsulosin is a **selective alpha-1A blocker**. Alpha-1A receptors are primarily located in the smooth muscle of the bladder neck and prostate. By blocking these, Tamsulosin causes muscle relaxation, improving urine flow in patients with **Benign Prostatic Hyperplasia (BPH)**. Unlike non-selective alpha-1 blockers, it has minimal effect on alpha-1B receptors (found in blood vessels), resulting in less orthostatic hypotension. **2. Analysis of Other Options:** * **Prazosin & Terazosin:** These are **non-selective alpha-1 blockers** (blocking 1A, 1B, and 1D subtypes). While they are used for BPH, they are also potent antihypertensives. In many MCQ formats, if a "uroselective" drug like Tamsulosin is present, it is highlighted for its specific clinical utility in BPH. * **Clonidine:** This is an **alpha-2 agonist** (central acting). It stimulates alpha-2 receptors in the medulla, decreasing sympathetic outflow, and is used as an antihypertensive. **3. NEET-PG High-Yield Pearls:** * **First-Dose Phenomenon:** Prazosin is notorious for causing marked orthostatic hypotension and syncope after the first dose. * **Uroselectivity:** Tamsulosin and Silodosin are the preferred "uroselective" agents for BPH because they do not require dose titration and have minimal cardiovascular side effects. * **IFIS:** Tamsulosin is associated with **Intraoperative Floppy Iris Syndrome (IFIS)** during cataract surgery; patients should inform their ophthalmologist if they are on this medication.

Q: Which of the following statements regarding the use of adrenaline in anaphylactic shock is true?

The usual dose is 0.5-1 mg by intramuscular route.. Adrenaline (Epinephrine) is the **drug of choice** for anaphylactic shock due to its rapid onset and multi-receptor action ($\alpha_1, \alpha_2, \beta_1, \beta_2$). ### **Explanation of Options** * **Option A (Correct):** The standard adult dose for anaphylaxis is **0.5 mg (range 0.3–0.5 mg)** of a **1:1000** solution administered via the **Intramuscular (IM)** route in the anterolateral thigh. IM is preferred over subcutaneous (SC) because it achieves higher and faster peak plasma concentrations. * **Option B (Incorrect):** While rare if dosed correctly, **cerebral hemorrhage** and cardiac arrhythmias are known life-threatening adverse effects of adrenaline, usually occurring due to rapid spikes in blood pressure if administered too quickly or in excessive doses. * **Option C (Incorrect):** Adrenaline has a very short half-life. In anaphylaxis, if the patient does not improve, the dose should be repeated every **5–15 minutes**, not every 2–4 hours. * **Option D (Incorrect):** The concentrations differ significantly. The **1:1000 (1 mg/ml)** solution is used for IM/SC routes. However, for **Intravenous (IV)** use, it must be diluted to **1:10,000 (0.1 mg/ml)** or even 1:100,000 to prevent fatal arrhythmias and severe hypertension. ### **High-Yield NEET-PG Pearls** * **Mechanism in Anaphylaxis:** $\alpha_1$ (vasoconstriction to treat hypotension/edema), $\beta_1$ (positive inotropy), and $\beta_2$ (bronchodilation and stabilization of mast cells). * **Route of Choice:** IM (Anterolateral thigh/Vastus lateralis) is the gold standard. * **Concentration Ratios:** * **1:1,000** = 1 mg in 1 ml (IM use) * **1:10,000** = 1 mg in 10 ml (IV use in Cardiac Arrest) * **Pediatric Dose:** 0.01 mg/kg (max 0.3 mg).

Q: Which of the following is a selective α2 agonist?

Clonidine. **Explanation:** **Clonidine** is the correct answer because it is a prototype **selective α2-adrenergic agonist**. It acts primarily on presynaptic α2 receptors in the brainstem (vasomotor center), leading to a decrease in sympathetic outflow. This reduction in norepinephrine release results in decreased peripheral vascular resistance and blood pressure. **Analysis of Incorrect Options:** * **Prazosin:** This is a selective **α1-blocker** (antagonist). It is primarily used in the treatment of hypertension and Benign Prostatic Hyperplasia (BPH) by causing vasodilation and relaxing prostatic smooth muscle. * **Adrenaline (Epinephrine):** This is a **non-selective adrenergic agonist** that acts on α1, α2, β1, and β2 receptors. Its effects are dose-dependent and widespread across the sympathetic nervous system. * **Propranolol:** This is a **non-selective β-blocker** (antagonist) that blocks both β1 and β2 receptors. It is used for hypertension, prophylaxis of migraine, and performance anxiety. **High-Yield Clinical Pearls for NEET-PG:** * **Other α2 Agonists:** Methyldopa (drug of choice for hypertension in pregnancy), Dexmedetomidine (used for sedation in ICU), and Tizanidine (centrally acting muscle relaxant). * **Side Effects of Clonidine:** Dry mouth (xerostomia), sedation, and most importantly, **rebound hypertension** if the drug is stopped abruptly. * **Diagnostic Use:** The Clonidine Suppression Test is used in the diagnosis of Pheochromocytoma (failure to suppress plasma catecholamines).

Q: Non-selective beta-blockers are contraindicated in patients with diabetes due to which of the following reasons?

Hypoglycemic unawareness. ### Explanation **1. Why Hypoglycemic Unawareness is Correct:** In diabetic patients, hypoglycemia (often caused by insulin or sulfonylureas) triggers a sympathetic "fight-or-flight" response. This results in warning signs like **tachycardia, palpitations, and tremors**, mediated by $\beta_1$ and $\beta_2$ receptors. Non-selective beta-blockers (e.g., Propranolol) block these receptors, masking these vital warning signs. Consequently, the patient may slide into a life-threatening hypoglycemic coma without realizing their blood glucose has dropped. This phenomenon is known as **hypoglycemic unawareness**. **2. Analysis of Incorrect Options:** * **A. Hyperglycemia:** Beta-blockers actually carry a risk of **hypoglycemia** (not hyperglycemia) because $\beta_2$ receptors are responsible for hepatic glycogenolysis and gluconeogenesis. Blocking them prevents the liver from releasing glucose during a crisis. * **C. Tachycardia:** While beta-blockers cause bradycardia, this is the *mechanism* of masking, not the *reason* for contraindication. The danger lies in the patient not feeling the tachycardia that should signal low blood sugar. * **D. Hypotension:** While beta-blockers can lower blood pressure, this is a therapeutic effect or a general side effect, not the specific reason they are contraindicated in diabetes. **3. High-Yield NEET-PG Pearls:** * **Sweating:** This is the only sympathetic symptom of hypoglycemia **not blocked** by beta-blockers, as it is mediated by **cholinergic** fibers (muscarinic receptors). * **Selective Beta-blockers:** Cardioselective ($\beta_1$) blockers like **Atenolol or Metoprolol** are preferred in diabetics if a beta-blocker is mandatory, as they have less effect on glucose metabolism and $\beta_2$-mediated symptoms. * **Delayed Recovery:** Non-selective blockers also delay recovery from hypoglycemia by inhibiting $\beta_2$-mediated compensatory glucose release.

Q: What is the action of 20mcg/kg/min dopamine?

Vasoconstriction. **Explanation:** The physiological effects of Dopamine are strictly **dose-dependent**, acting on different receptors as the infusion rate increases. This is a high-yield concept for NEET-PG, often referred to as the "Dopamine Dose Ladder." 1. **Why Vasoconstriction is correct:** At high doses (**>10–15 mcg/kg/min**, and specifically at 20 mcg/kg/min), dopamine loses its selectivity for dopaminergic and beta-receptors. It predominantly stimulates **Alpha-1 adrenergic receptors**, leading to potent peripheral vasoconstriction [1]. This increases systemic vascular resistance (SVR). 2. **Analysis of Incorrect Options:** * **Option A (Renal vasodilation):** This occurs at **low doses (0.5–2 mcg/kg/min)** via D1 receptors in the renal vasculature. While it increases renal blood flow, clinical studies have shown it does not prevent acute kidney injury. * **Option D (Increased myocardial contractility):** This occurs at **medium doses (2–10 mcg/kg/min)** via **Beta-1 receptors**. This increases heart rate and stroke volume (inotropic effect). * **Option C (Increased blood pressure):** While high-dose dopamine *does* increase blood pressure, "Vasoconstriction" is the more precise physiological **action** requested by the question. Blood pressure elevation is the *result* of the vasoconstriction and increased cardiac output. **High-Yield Clinical Pearls for NEET-PG:** * **Low Dose (D1):** "Renal dose" (Vasodilation). * **Medium Dose (B1):** "Cardiac dose" (Inotropy). * **High Dose (A1):** "Pressor dose" (Vasoconstriction). * **Antidote:** If extravasation occurs during high-dose infusion, **Phentolamine** (alpha-blocker) is used to prevent tissue necrosis.

Q: Which one of the following is not an alpha-adrenoceptor agonist?

Methyldopa. **Explanation:** The core concept tested here is the difference between a **direct agonist** and a **prodrug**. **Why Methyldopa is the correct answer:** Methyldopa is not an alpha-adrenoceptor agonist itself. Instead, it is a **prodrug**. Once it crosses the blood-brain barrier, it is converted into **$\alpha$-methylnorepinephrine** by the enzymes DOPA decarboxylase and Dopamine $\beta$-hydroxylase. It is this active metabolite, not Methyldopa, that acts as a potent agonist at central $\alpha_2$ receptors to decrease sympathetic outflow. **Analysis of Incorrect Options:** * **Clonidine:** A direct-acting, selective $\alpha_2$-adrenoceptor agonist. It acts on the imidazoline receptors and $\alpha_2$ receptors in the nucleus tractus solitarius to reduce blood pressure. * **Guanabenz and Guanfacine:** These are also direct-acting central $\alpha_2$-adrenoceptor agonists. They share a similar mechanism of action to clonidine but are used less frequently in clinical practice. **High-Yield NEET-PG Clinical Pearls:** 1. **Drug of Choice:** Methyldopa remains the drug of choice for **Pregnancy-Induced Hypertension (PIH)** due to its long-term safety profile for the fetus. 2. **Side Effects:** A classic side effect of Methyldopa is a **positive Coombs test**, which may rarely lead to hemolytic anemia. 3. **Rebound Hypertension:** Abrupt withdrawal of direct $\alpha_2$ agonists like Clonidine can lead to a hypertensive crisis due to a sudden surge in catecholamines. 4. **Mechanism:** All four drugs listed decrease sympathetic tone, but only Methyldopa requires metabolic conversion to do so.

Q: Cholinergic drugs are used in all the following conditions except?

Bradycardia. **Explanation:** The correct answer is **Bradycardia** because cholinergic drugs (parasympathomimetics) stimulate the M2 receptors in the heart, leading to a decrease in heart rate (negative chronotropy). Therefore, they are **contraindicated** in bradycardia. Instead, anticholinergic drugs like Atropine are the treatment of choice for symptomatic bradycardia. **Analysis of Options:** * **Cobra Bite:** Cobra venom contains post-synaptic neurotoxins that block Nicotinic receptors (Nm) at the neuromuscular junction, causing paralysis. Cholinesterase inhibitors like **Neostigmine** are used to increase Acetylcholine levels, which compete with the toxin to reverse muscle weakness. * **Postoperative paralytic ileus:** Cholinergic agonists (e.g., **Bethanechol**) or cholinesterase inhibitors (e.g., **Neostigmine**) stimulate M3 receptors on the gastrointestinal smooth muscle, promoting motility and helping resolve non-obstructive ileus or urinary retention. * **Glaucoma:** Miotics like **Pilocarpine** cause contraction of the iris sphincter (miosis) and the ciliary muscle. This opens the trabecular meshwork, facilitating the drainage of aqueous humor and reducing intraocular pressure. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Atropine is the DOC for sinus bradycardia and organophosphate poisoning. * **Bethanechol** is the preferred cholinergic for bladder atony because it has negligible effects on the heart (M2) but high selectivity for the gut and bladder (M3). * **Neostigmine** is always co-administered with Glycopyrrolate or Atropine to prevent unwanted muscarinic side effects (like bradycardia) when reversing neuromuscular blockade.

Question 1

Which skeletal muscle relaxant causes significant release of histamine?

Accepted Answer

D-tubocurarine

Answer

Pancuronium

Answer

Atracurium

Answer

Gallamine

Question 2

Reflex tachycardia is most likely to occur after the systemic administration of which of the following drugs?

Accepted Answer

albuterol

Answer

methoxamine

Answer

phenylephrine

Answer

propranolol

Question 3

Which of the following is an alpha-1 blocker?

Accepted Answer

Tamsulosin

Answer

Prazosin

Answer

Terazosin

Answer

Clonidine

Question 4

Which of the following statements regarding the use of adrenaline in anaphylactic shock is true?

Accepted Answer

The usual dose is 0.5-1 mg by intramuscular route.

Answer

Cerebral hemorrhage never occurs as an adverse effect to epinephrine when used in the treatment of anaphylactic shock.

Answer

It is repeated after every 2-4 hours.

Answer

The same solution can be given for subcutaneous as well as intravenous routes.

Question 5

Exogenous adrenaline is metabolized by which of the following?

Accepted Answer

COMT (Catechol-O-methyltransferase)

Answer

Acetyltransferase

Answer

Reuptake

Answer

AchE (Acetylcholinesterase)

Question 6

Which of the following is a selective α2 agonist?

Accepted Answer

Clonidine

Answer

Prazosin

Answer

Adrenaline

Answer

Propranolol

Question 7

Non-selective beta-blockers are contraindicated in patients with diabetes due to which of the following reasons?

Accepted Answer

Hypoglycemic unawareness

Answer

Hyperglycemia

Answer

Tachycardia

Answer

Hypotension

Question 8

What is the action of 20mcg/kg/min dopamine?

Accepted Answer

Vasoconstriction

Answer

Renal vasodilation

Answer

Increased blood pressure

Answer

Increased myocardial contractility

Question 9

Which one of the following is not an alpha-adrenoceptor agonist?

Accepted Answer

Methyldopa

Answer

Clonidine

Answer

Guanabenz

Answer

Guanfacine

Question 10

Cholinergic drugs are used in all the following conditions except?

Accepted Answer

Bradycardia

Answer

Cobra Bite

Answer

Postoperative paralytic ileus

Answer

Glaucoma

Autonomic Nervous System Drugs — MCQs

Autonomic Nervous System Drugs — MCQs

On this page

Practice by Chapter

Want unlimited practice?