Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology Indian Medical PG Practice Questions and MCQs

Question 391: What is the typical resting membrane potential (RMP) of smooth muscle cells?

A. -90 mV
B. -70 mV
C. -60 mV (Correct Answer)
D. -40 mV

Explanation: ***-60 mV*** - Smooth muscle cells typically have a **resting membrane potential of -55 to -60 mV**, which is **less negative** compared to skeletal muscle (-90 mV) or neurons (-70 mV). - This relatively depolarized RMP allows them to be **more easily excited** and enables **spontaneous slow wave depolarizations** and pacemaker activity in some smooth muscle types. - The less negative potential is due to higher resting permeability to Na+ and Ca2+ compared to skeletal muscle. *-90 mV* - This is the typical resting membrane potential for **skeletal muscle cells** and **large myelinated nerve fibers**. - Such a highly negative RMP provides a **larger buffer against accidental excitation** and ensures precise voluntary control. - This value is maintained by high K+ permeability and active Na+/K+ ATPase activity. *-70 mV* - This is the characteristic resting membrane potential of **most neurons**, allowing for efficient generation and propagation of action potentials. - It represents a balance between depolarizing and hyperpolarizing influences, optimal for neuronal signaling. - This is more negative than smooth muscle but less negative than skeletal muscle. *-40 mV* - This value is **too depolarized** to be a stable resting potential for smooth muscle and would be **near threshold potential**. - At -40 mV, voltage-gated calcium channels would be significantly activated, causing sustained contraction rather than a resting state. - This might represent a **partially depolarized state** or the RMP of specialized pacemaker cells like cardiac SA node cells, but **not typical smooth muscle**.

Question 392: Which of the following statements is true regarding smooth muscle contraction?

A. None of the options.
B. Calmodulin plays no role in smooth muscle contraction.
C. Phosphorylation of myosin is essential for contraction. (Correct Answer)
D. Troponin plays a significant role in smooth muscle contraction.

Explanation: **Phosphorylation of myosin is essential for contraction.** - In **smooth muscle**, the **myosin light chain (MLC)** must be phosphorylated by **myosin light chain kinase (MLCK)** to enable interaction with actin and initiate contraction. - This phosphorylation causes a conformational change in the **myosin head**, increasing its ATPase activity and allowing cross-bridge cycling. *Calmodulin plays no role in smooth muscle contraction.* - **Calmodulin (CaM)** is crucial for smooth muscle contraction, as it binds **calcium ions (Ca²⁺)** forming a Ca²⁺-CaM complex. - This complex then activates **myosin light chain kinase (MLCK)**, which phosphorylates myosin, triggering contraction. *None of the options.* - This statement is incorrect because one of the provided options, "Phosphorylation of myosin is essential for contraction," is indeed true. *Troponin plays a significant role in smooth muscle contraction.* - Unlike **striated muscle (skeletal and cardiac)**, **smooth muscle** does not contain **troponin**. - Regulation of smooth muscle contraction is primarily **calcium-calmodulin-dependent**, with roles for **MLCK** and **MLCP**, rather than troponin.

Question 393: 'Flare' in Triple response is mediated by :

A. Axon reflex (Correct Answer)
B. Arteriolar dilation
C. Histamine release
D. Local hormones

Explanation: ***Axon reflex*** - The "flare" component of the triple response is caused by an **axon reflex**, where sensory nerve endings release **vasoactive neuropeptides** such as substance P and calcitonin gene-related peptide (CGRP). - These neuropeptides cause **vasodilation** in the surrounding area, leading to the characteristic red, irregularly shaped halo around the wheal. *Arteriolar dilation* - While arteriolar dilation is a component of the triple response and contributes to the **redness (flush)** and **flare**, it is not the direct mediator of the flare itself. - The initial arteriolar dilation is primarily due to **histamine** acting directly on the vessels, whereas the flare is a broader, neurally mediated spread of vasodilation. *Histamine release* - **Histamine** release from mast cells is the primary mediator of the initial **redness (flush)** and the formation of the **wheal** (swelling due to capillary permeability). - While histamine plays a role in the overall response, it does not directly mediate the "flare" component, which involves neuronal signaling via the axon reflex. *Local hormones* - While various **local mediators** (which could be broadly considered "local hormones" in a sense) are involved in inflammatory responses, the specific term "local hormones" is too general and does not precisely describe the mechanism of the flare. - The axon reflex, involving specific **neuropeptides**, is the precise mechanism for the flare, not a general category of local hormones.

Question 394: Maximum density of muscle spindle is found in?

A. Calf muscle
B. Lumbricals (Correct Answer)
C. Triceps
D. Quadriceps muscle

Explanation: ***Lumbricals*** - **Lumbricals** are small, intricate muscles in the hand, responsible for fine motor control and precise movements like grasping and manipulating objects. - The high density of **muscle spindles** in lumbricals allows for extremely accurate feedback on muscle length and tension, crucial for **proprioception** and delicate tasks. *Calf muscle* - **Calf muscles** (gastrocnemius and soleus) are large muscles primarily involved in powerful movements like walking and running. - While they do contain muscle spindles for proprioception, their density is lower compared to muscles involved in fine motor control. *Quadriceps muscle* - The **quadriceps femoris** is a large muscle group in the thigh responsible for knee extension and powerful leg movements. - They contain muscle spindles to monitor muscle stretch, but not with the extreme density seen in muscles with fine motor functions. *Triceps* - The **triceps brachii** is a large muscle on the back of the upper arm, primarily responsible for elbow extension. - It has a moderate density of muscle spindles, sufficient for coordinating arm movements but not as high as muscles designed for precision.

Question 395: Which of the following statements about the oculocardiac reflex is false?

A. It is mediated by trigeminal and vagus nerve.
B. Reflex is more sensitive in neonates
C. It is characterized by bradycardia following traction on extra- ocular muscles
D. It is mediated by oculomotor and vagus nerve (Correct Answer)

Explanation: ***It is mediated by oculomotor and vagus nerve*** - The oculocardiac reflex (OCR) is classically mediated by the **trigeminal nerve (afferent)** and the **vagus nerve (efferent)**, not the oculomotor nerve. - Stimulation of the trigeminal sensory afferents from the eye leads to an efferent vagal response, causing a decrease in heart rate. *It is mediated by trigeminal and vagus nerve.* - This statement accurately describes the neural pathways involved in the oculocardiac reflex, where the **trigeminal nerve acts as the afferent limb** and the **vagus nerve acts as the efferent limb**. - Stimulation of ocular structures activates trigeminal nerve endings, which transmit signals to the brainstem, leading to vagal stimulation and subsequent cardiac effects. *Reflex is more sensitive in neonates* - The oculocardiac reflex is indeed more pronounced and easily triggered in **neonates and young children** due to their relatively immature autonomic nervous system. - This increased sensitivity makes them more susceptible to **bradycardia** during ophthalmic procedures. *It is characterized by bradycardia following traction on extra- ocular muscles* - The classic manifestation of the oculocardiac reflex is **bradycardia** (slowing of the heart rate) in response to stimuli such as pressure on the eyeball or traction on the extraocular muscles. - Other possible manifestations include **arrhythmias**, **asystole**, and hypotension, although bradycardia is the most common.

Question 396: Which part of the sympathetic nervous system is responsible for secreting catecholamines?

A. Cardiac ganglion
B. Cervical sympathetic chain
C. Adrenal medulla (Correct Answer)
D. Thoracic sympathetic chain

Explanation: ***Adrenal medulla*** - The adrenal medulla acts as a modified **sympathetic ganglion**, directly innervated by **preganglionic sympathetic fibers**. - Upon stimulation, it releases a high concentration of **epinephrine** (adrenaline) and a smaller amount of **norepinephrine** (noradrenaline) into the bloodstream, acting as hormones. *Cardiac ganglion* - **Cardiac ganglia** are parasympathetic ganglia located in the heart, involved in regulating heart rate and contractility via acetylcholine release. - They do not secrete **catecholamines** but rather act as relay stations for parasympathetic innervation. *Cervical sympathetic chain* - The **cervical sympathetic chain** primarily innervates structures in the head, neck, and upper limbs, influencing functions like pupils, salivary glands, and sweat glands. - While it contains sympathetic neurons, its primary role is not the systemic release of **catecholamines** into the bloodstream. *Thoracic sympathetic chain* - The **thoracic sympathetic chain** provides sympathetic innervation to organs in the thoracic and abdominal cavities, influencing heart rate, bronchodilation, and visceral blood flow. - Like other sympathetic ganglia, it releases norepinephrine at target organ synapses, but it does not serve as a major endocrine gland for systemic catecholamine release.

Question 397: What does the transient response observed during the insertion of an electrode in electromyography (EMG) indicate?

A. Spontaneous muscle activity
B. Voluntary muscle contraction
C. Cell membrane disruption (Correct Answer)
D. Induced muscle contraction

Explanation: **Cell membrane disruption** - The **transient response** observed during electrode insertion in **EMG** is caused by the mechanical trauma of the needle disrupting the **muscle fiber cell membranes**. - This disruption leads to a brief depolarization and subsequent repolarization of the affected fibers, generating characteristic electrical activity. *Spontaneous muscle activity* - **Spontaneous muscle activity**, such as **fibrillation potentials** or **positive sharp waves**, occurs independently of electrode insertion. - While observed during EMG, these are indicative of **denervation** or **myopathy** and are not directly caused by the act of insertion itself. *Voluntary muscle contraction* - **Voluntary muscle contraction** is recorded when the patient actively contracts the muscle and results in **motor unit action potentials (MUAPs)**. - This is a distinct process from the transient activity produced by electrode insertion. *Induced muscle contraction* - **Induced muscle contraction** typically refers to activity caused by **nerve stimulation** (e.g., in nerve conduction studies) or direct electrical stimulation of the muscle. - This is not the mechanism for the transient response during simple electrode insertion.

Question 398: Which of the following is a potassium Channelopathy?

A. Hyperkalemic periodic paralysis
B. Long QT-syndrome
C. Episodic ataxia I (Correct Answer)
D. Hypokalemic periodic paralysis

Explanation: ***Episodic ataxia I*** - This condition is caused by mutations in the **KCNA1 gene**, which encodes the **Kv1.1 voltage-gated potassium channel**. - It represents a **classic neuromuscular potassium channelopathy** with episodes of **ataxia**, **dysarthria**, and myokymia. - This is a pure potassium channelopathy affecting the nervous system. *Hyperkalemic periodic paralysis* - This condition is caused by mutations in the **SCN4A gene**, which encodes a **sodium channel** subunit in skeletal muscle. - Despite the name suggesting potassium involvement, it is a **sodium channelopathy**, not a potassium channelopathy. - Episodes are triggered by elevated serum potassium levels. *Long QT syndrome* - Several subtypes (LQT1, LQT2, LQT5) are indeed caused by mutations in **potassium channel genes** (KCNQ1, KCNH2, KCNE1). - However, Long QT syndrome is a **heterogeneous group** that also includes sodium (LQT3) and calcium channelopathies. - It is classified as a **cardiac channelopathy** affecting ventricular repolarization. - In the context of this question, **Episodic ataxia I** is the most specific example of a pure potassium channelopathy. *Hypokalemic periodic paralysis* - This condition is most commonly caused by mutations in the **CACNA1S gene** (encoding a **calcium channel**) or **SCN4A gene** (encoding a **sodium channel**). - It is not a potassium channelopathy despite the hypokalemia that triggers episodes.

Question 399: What is another name for the withdrawal reflex?

A. Golgi tendon reflex
B. Extension reflex
C. Stretch reflex
D. Flexor reflex (Correct Answer)

Explanation: ***Flexor reflex*** - The withdrawal reflex is also known as the **flexor reflex** because it causes the rapid flexion (bending) of a limb to withdraw it from a noxious stimulus. - This reflex is a **polysynaptic reflex** involving interneurons in the spinal cord. *Golgi tendon reflex* - The **Golgi tendon reflex** is a protective reflex that causes muscle relaxation in response to excessive muscle tension. - It involves activation of **Golgi tendon organs**, which are proprioceptors located in the tendons. *Extension reflex* - The **extension reflex** is typically observed in withdrawal reflexes of the opposing limb, known as the **crossed extensor reflex**, to maintain balance. - It involves the extension of the contralateral limb while the ipsilateral limb flexes. *Stretch reflex* - The **stretch reflex** (or myotatic reflex) causes muscle contraction in response to stretching of the muscle. - It is a **monosynaptic reflex** involving muscle spindles and maintaining muscle tone.

Question 400: Which of the following is an action of muscarinic cholinergic receptors?

A. Skeletal muscle contraction
B. Acid secretion in stomach
C. Decreased heart rate (Correct Answer)
D. Salivation and lacrimation

Explanation: ***Decreased heart rate*** - Activation of **muscarinic cholinergic receptors (M2 receptors)** in the heart leads to a decrease in heart rate and conduction velocity. - This effect is mediated by the **vagus nerve (parasympathetic nervous system)**, which releases acetylcholine to act on these receptors. - This is the **most characteristic and clinically significant cardiovascular effect** of muscarinic receptor activation, making it the expected answer. *Skeletal muscle contraction* - **Skeletal muscle contraction** is mediated by **nicotinic acetylcholine receptors (nAChRs)** at the **neuromuscular junction**, NOT muscarinic receptors. - Nicotinic receptors are **ligand-gated ion channels** that cause direct depolarization and muscle contraction when activated. - This is the only option that is **NOT a muscarinic receptor action**. *Acid secretion in stomach* - **Gastric acid secretion** IS mediated by **M3 muscarinic receptors** on parietal cells. - Acetylcholine from the vagus nerve directly stimulates parietal cells and also stimulates histamine release from enterochromaffin-like cells. - While this is a valid muscarinic action, in the context of distinguishing muscarinic effects, **cardiac effects** (decreased heart rate) are more emphasized as the classic teaching point. *Salivation and lacrimation* - **Salivation and lacrimation** ARE mediated by **M3 muscarinic receptors** in exocrine glands. - These are classic parasympathetic/muscarinic effects taught in physiology. - However, when distinguishing key muscarinic actions, **M2 receptor-mediated cardiac effects** are typically highlighted as the primary cardiovascular manifestation, while M3 effects on glands are secondary teaching points.

Practice by Chapter

Resting Membrane Potential

Practice Questions

Action Potential Generation and Propagation

Practice Questions

Neuromuscular Junction

Practice Questions

Skeletal Muscle Contraction

Practice Questions

Smooth Muscle Physiology

Practice Questions

Cardiac Muscle Properties

Practice Questions

Muscle Metabolism and Fatigue

Practice Questions

Motor Unit Function

Practice Questions

Neurotransmitters and Receptors

Practice Questions

Electrophysiological Measurements

Practice Questions

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