Autonomic Nervous System Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Autonomic Nervous System. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Autonomic Nervous System Indian Medical PG Question 1: Which of the following conditions is primarily treated by sympathectomy?
- A. Buerger's disease
- B. Acrocyanosis
- C. Hyperhidrosis (Correct Answer)
- D. Raynaud's disease
Autonomic Nervous System Explanation: ***Hyperhidrosis***
- **Sympathectomy** (especially thoracic sympathectomy) is a definitive treatment for severe, localized **hyperhidrosis** (excessive sweating) that has not responded to conservative therapies.
- The procedure aims to interrupt the sympathetic nerves responsible for stimulating sweat glands, commonly in the palms, soles, or axillae.
*Buerger's disease*
- While **sympathectomy** was historically used, its efficacy in **Buerger's disease** (thromboangiitis obliterans) is questionable and largely replaced by smoking cessation and other treatments for limb salvage.
- The primary issue is **inflammation** and **thrombosis** of small and medium-sized arteries and veins, not primarily sympathetic overactivity.
*Acrocyanosis*
- **Acrocyanosis** is a benign condition characterized by persistent, painless, blue discoloration of the extremities due to vasospasm of small skin arteries and arterioles.
- Treatment is generally reassurance and avoidance of cold, and **sympathectomy** is rarely, if ever, indicated or effective due to the non-progressive and cosmetic nature of the condition.
*Raynaud's disease*
- **Raynaud's disease** is a vasospastic disorder, but **sympathectomy** is usually reserved for severe cases with impending tissue loss or critical ischemia that fail medical management.
- Medical management with calcium channel blockers is the primary treatment, as the condition involves episodic vasospasm of digital arteries.
Autonomic Nervous System Indian Medical PG Question 2: All of the following are trigeminal autonomic cephalgias except
- A. Short lasting unilateral neuralgiform headache attacks
- B. Tension type headache (Correct Answer)
- C. Episodic cluster headache
- D. Paroxysmal hemicranias
Autonomic Nervous System Explanation: ***Tension type headache***
- **Tension-type headaches** are characterized by a bilateral, pressing, or tightening quality, *without* the prominent autonomic symptoms seen in trigeminal autonomic cephalgias [1].
- They are generally not associated with activation of the **trigeminal autonomic reflex**, which is central to TACs.
*Short lasting unilateral neuralgiform headache attacks*
- These are characterized by **short-lasting** attacks of severe, unilateral head pain accompanied by **prominent trigeminal autonomic features**.
- This category includes SUNCT (Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing) and SUNA (Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms) and are indeed trigeminal autonomic cephalgias.
*Episodic cluster headache*
- **Cluster headaches** are the most well-known of the trigeminal autonomic cephalgias, characterized by severe, unilateral pain in the orbital, supraorbital, or temporal regions [1].
- They are invariably accompanied by **ipsilateral autonomic symptoms** like lacrimation, conjunctival injection, nasal congestion, and ptosis [2].
*Paroxysmal hemicranias*
- This condition involves frequent, short-lasting attacks of **severe, unilateral pain** typically in the orbital, supraorbital, or temporal regions.
- It is consistently associated with prominent **ipsilateral autonomic features** and shows an absolute response to **indomethacin**, distinguishing it from other TACs.
Autonomic Nervous System Indian Medical PG Question 3: TRUE statement regarding nerve supply of adrenal gland:
- A. Adrenal cortex has no nerve supply
- B. Adrenal medulla has no nerve supply
- C. Release of catecholamines is not affected by nerve supply
- D. Preganglionic fibres from lower thoracic spinal segments bypass sympathetic chain (Correct Answer)
Autonomic Nervous System Explanation: ***Preganglionic fibres from lower thoracic & upper lumbar spinal segments bypass sympathetic chain***
- The adrenal medulla is innervated by **preganglionic sympathetic fibers** originating from the **T5-T11 spinal cord segments**, which travel through the splanchnic nerves and synapse directly on chromaffin cells, effectively bypassing the sympathetic chain ganglia [1], [2].
- This direct innervation allows for a **rapid, systemic catecholamine release** in response to stress.
*Adrenal cortex has no nerve supply*
- The **adrenal cortex** receives some **autonomic innervation**, primarily sympathetic, though it is less dense and its direct role in steroidogenesis is not fully understood.
- While hormonal signals are primary for cortical regulation, nerve fibers are present and may modulate blood flow or cellular activity.
*Adrenal medulla has no nerve supply*
- The **adrenal medulla** is a modified sympathetic ganglion whose **chromaffin cells** are directly innervated by **preganglionic sympathetic fibers** [1], [2].
- This direct neural input is crucial for its rapid response in releasing **catecholamines** into the bloodstream.
*Release of catecholamines is not affected by nerve supply*
- The release of **catecholamines** (epinephrine and norepinephrine) from the **adrenal medulla** is directly and primarily controlled by **preganglionic sympathetic innervation** [1], [2].
- Without this nerve supply, the stress-induced release of these hormones would be severely impaired, highlighting the critical role of neural input.
Autonomic Nervous System Indian Medical PG Question 4: Mechanism by which Ach decreases heart rate is by:
- A. Prolongation of action potential duration
- B. Reduction in calcium influx
- C. Inhibition of sympathetic activity
- D. Delayed diastolic depolarization (Correct Answer)
Autonomic Nervous System Explanation: ***Delayed diastolic depolarization***
- Acetylcholine (ACh) binding to muscarinic receptors on nodal cells increases **potassium permeability**, leading to a more negative maximal diastolic potential.
- This slows the rate of **spontaneous depolarization** (pacemaker potential), thereby delaying the point at which the threshold for an action potential is reached and reducing heart rate.
*Prolongation of action potential duration*
- ACh typically **shortens** the action potential duration in atrial and nodal cells by increasing potassium efflux, which hyperpolarizes the cell and hastens repolarization.
- A prolonged action potential duration would generally lead to a **slower heart rate** by increasing the refractory period, but this is achieved through different ionic mechanisms and is not the primary mechanism of ACh.
*Reduction in calcium influx*
- While ACh does reduce the inward **calcium current (ICa)** in nodal cells, contributing to a slower heart rate and weaker contractility, this effect primarily influences the upstroke and peak of the action potential.
- The more **fundamentally important mechanism** for heart rate reduction is the impact on the pacemaker potential's slope, which is governed by altered ion conductances, predominantly potassium.
*Inhibition of sympathetic activity*
- ACh acts directly on **muscarinic receptors** on cardiac cells to decrease heart rate, which is a parasympathetic effect.
- It does not directly inhibit sympathetic nerve activity but rather **counteracts sympathetic effects** by directly modulating cardiac cell physiology.
Autonomic Nervous System Indian Medical PG Question 5: Effects of beta blockers on the heart are all of the following except:
- A. Decreases duration of systole (Correct Answer)
- B. Decrease in heart rate
- C. May decrease cardiac output initially.
- D. May precipitate heart failure in acute settings.
Autonomic Nervous System Explanation: ***Decreases duration of systole***
- Beta-blockers primarily prolong the **duration of systole** by extending the **ejection time** and slowing ventricular relaxation.
- They also increase the **diastolic filling time** by reducing heart rate, impacting overall cardiac cycle duration.
*Decrease in heart rate*
- Beta-blockers block **beta-1 adrenergic receptors** in the heart, leading to a decrease in **sympathetic stimulation** and thus a reduced heart rate.
- This effect is beneficial in conditions like **tachycardia** and **angina**, as it reduces myocardial oxygen demand.
*May decrease cardiac output initially.*
- By reducing heart rate and contractility, beta-blockers can initially decrease **cardiac output**, especially in patients with pre-existing **ventricular dysfunction**.
- This effect is often transient, as chronic use can lead to beneficial remodeling and improved efficiency in some conditions.
*May precipitate heart failure in acute settings.*
- In patients with acutely decompensated heart failure or severe left ventricular dysfunction, beta-blockers can acutely worsen cardiac function due to their **negative inotropic effects**.
- Therefore, beta-blockers are typically initiated cautiously at low doses in stable heart failure patients and are contraindicated in acute decompensation.
Autonomic Nervous System Indian Medical PG Question 6: Which of the following does not have sympathetic noradrenergic fibers?
- A. Heart
- B. Eye
- C. Sweat gland (Correct Answer)
- D. Blood vessels
Autonomic Nervous System Explanation: ***Sweat gland***
- While sweat glands are innervated by the **sympathetic nervous system**, their postganglionic fibers are **cholinergic**, releasing **acetylcholine** rather than noradrenaline.
- This is an important exception where sympathetic stimulation leads to acetylcholine release, causing sweating.
*Blood vessels*
- Most blood vessels, particularly resistance vessels such as **arterioles**, receive substantial **sympathetic noradrenergic innervation** that causes vasoconstriction.
- This sympathetic tone is crucial for regulating **blood pressure** and distributing blood flow.
*Heart*
- The heart is richly innervated by **sympathetic noradrenergic fibers** that increase **heart rate**, **contractility**, and **conduction velocity** via beta-1 adrenergic receptors.
- This makes noradrenaline a key neurotransmitter in the sympathetic regulation of cardiac function.
*Eye*
- The eye receives sympathetic noradrenergic innervation primarily to the **dilator pupillae muscle**, causing **mydriasis** (pupil dilation) upon activation.
- These fibers also contribute to the sympathetic control of the **tarsal muscle** (Müller's muscle) in the eyelid.
Autonomic Nervous System Indian Medical PG Question 7: Match the following:
A) Glossopharyngeal nerve
B) Spinal accessory nerve
C) Facial nerve
D) Mandibular nerve
1) Shrugging of shoulder
2) Touch sensation from the posterior one-third of the tongue
3) Chewing
4) Taste from the anterior two-thirds of the tongue
- A. A-3 , B-1 , C-4 , D-2
- B. A-2 , B-3 , C-4 , D-1
- C. A-4 , B-1 , C-2 , D-3
- D. A-2 , B-1 , C-4 , D-3 (Correct Answer)
Autonomic Nervous System Explanation: ***A-2 , B-1 , C-4 , D-3***
- **A) Glossopharyngeal nerve (CN IX)** is responsible for **general sensation and taste from the posterior one-third of the tongue** [1]. (2).
- **B) Spinal Accessory nerve (CN XI)** innervates the **sternocleidomastoid** and **trapezius muscles**, which are involved in shrugging the shoulders (1).
- **C) Facial nerve (CN VII)** carries **taste sensation from the anterior two-thirds of the tongue** [1] (4) via the chorda tympani.
- **D) Mandibular nerve (V3)**, a branch of the trigeminal nerve, innervates the muscles of mastication, enabling **chewing** (3).
*A-3 , B-1 , C-4 , D-2*
- This option incorrectly associates the **glossopharyngeal nerve** with chewing, which is a function of the mandibular nerve (V3).
- It also incorrectly associates the **mandibular nerve** with touch sensation from the posterior one-third of the tongue, which is a function of the glossopharyngeal nerve [1].
*A-2 , B-3 , C-4 , D-1*
- This option incorrectly links the **spinal accessory nerve** with chewing; this nerve primarily controls shoulder and neck movements.
- It also incorrectly assigns shrugging of the shoulder to the **mandibular nerve** instead of the spinal accessory nerve.
*A-4 , B-1 , C-2 , D-3*
- This choice incorrectly attributes **taste from the anterior two-thirds of the tongue** to the glossopharyngeal nerve, which supplies the posterior one-third [1].
- It also incorrectly links **touch sensation from the posterior one-third of the tongue** to the facial nerve, which is involved in taste from the anterior two-thirds [1].
Autonomic Nervous System Indian Medical PG Question 8: Which neurotransmitter is associated with parasympathetic stimulation?
- A. Serotonin
- B. Dopamine
- C. Glutamate
- D. Acetylcholine (Correct Answer)
Autonomic Nervous System Explanation: ***Acetylcholine***
- **Acetylcholine** is the primary neurotransmitter released by postganglionic neurons in the **parasympathetic nervous system**, mediating its effects on target organs
- It acts on **muscarinic receptors** (at target organs) and **nicotinic receptors** (at ganglia) to produce characteristic "rest and digest" responses like decreased heart rate, increased digestive activity, pupillary constriction, and increased glandular secretions
- Both preganglionic and postganglionic parasympathetic neurons release acetylcholine (cholinergic transmission)
*Serotonin*
- **Serotonin** (5-HT) is a monoamine neurotransmitter primarily involved in mood regulation, sleep, appetite, and gut motility
- While it modulates some autonomic functions, it is not the primary effector neurotransmitter for the parasympathetic system
*Dopamine*
- **Dopamine** is a catecholamine neurotransmitter known for its role in reward, motivation, motor control, and executive functions
- It plays a role in the sympathetic nervous system in some contexts (e.g., renal blood flow regulation at low doses) but is not associated with parasympathetic stimulation
*Glutamate*
- **Glutamate** is the main excitatory neurotransmitter in the central nervous system, crucial for learning and memory
- It has no direct role in the peripheral parasympathetic nervous system
Autonomic Nervous System Indian Medical PG Question 9: All of the following are seen in the Horner's syndrome, Except
- A. Dilated pupil (Correct Answer)
- B. Drooping of upper eyelid
- C. Enophthalmos
- D. Loss of sweating on same side of face
Autonomic Nervous System Explanation: ***Dilated pupil***
- **Horner's syndrome** results from damage to the sympathetic pathway, leading to **miosis** (constricted pupil) due to unopposed parasympathetic activity [2].
- A **dilated pupil** would be indicative of a different pathology, such as oculomotor nerve palsy [3].
*Drooping of upper eyelid*
- This symptom, known as **ptosis**, is a classic feature of Horner's syndrome due to the paralysis of the **superior tarsal muscle** (Müller's muscle), which is innervated by the sympathetic nervous system [1], [2].
- The degree of ptosis is typically mild to moderate.
*Enophthalmos*
- **Enophthalmos**, or the apparent sinking of the eyeball into the orbit, is often seen in Horner's syndrome.
- This is partly an illusion caused by the ptosis and sometimes attributed to a loss of tone in the **orbitalis muscle** (if present and sympathetically innervated).
*Loss of sweating on same side of face*
- This is known as **anhydrosis** and occurs on the **ipsilateral side of the face and neck** due to the disruption of sympathetic innervation to the sweat glands.
- The extent of anhydrosis depends on the level of the lesion along the sympathetic pathway [4].
Autonomic Nervous System Indian Medical PG Question 10: Match the following drugs in Column A with their contraindications in Column B.
| Column A | Column B |
| :-- | :-- |
| 1. Morphine | 1. QT prolongation |
| 2. Amiodarone | 2. Thromboembolism |
| 3. Vigabatrin | 3. Pregnancy |
| 4. Estrogen preparations | 4. Head injury |
- A. A-1, B-3, C-2, D-4
- B. A-4, B-1, C-3, D-2 (Correct Answer)
- C. A-3, B-2, C-4, D-1
- D. A-2, B-4, C-1, D-3
Autonomic Nervous System Explanation: ***A-4, B-1, C-3, D-2***
- **Morphine** is contraindicated in **head injury** as it can increase intracranial pressure and mask neurological symptoms.
- **Amiodarone** is contraindicated in patients with **QT prolongation** due to its risk of inducing more severe arrhythmias like Torsades de Pointes.
- **Vigabatrin** is contraindicated during **pregnancy** due to its potential for teratogenicity and adverse effects on fetal development.
- **Estrogen preparations** are contraindicated in patients with a history of **thromboembolism** due to their increased risk of blood clot formation.
*A-1, B-3, C-2, D-4*
- This option incorrectly matches **Morphine** with QT prolongation and **Estrogen preparations** with head injury, which are not their primary contraindications.
- It also incorrectly links **Vigabatrin** with thromboembolism and **Amiodarone** with pregnancy.
*A-3, B-2, C-4, D-1*
- This choice incorrectly associates **Morphine** with pregnancy and **Vigabatrin** with head injury, which are not the most critical or direct contraindications.
- It also misaligns **Amiodarone** with thromboembolism and **Estrogen preparations** with QT prolongation.
*A-2, B-4, C-1, D-3*
- This option incorrectly matches **Morphine** with thromboembolism and **Amiodarone** with head injury, which are not their most significant contraindications.
- It also incorrectly links **Vigabatrin** with QT prolongation and **Estrogen preparations** with pregnancy.
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