Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology Indian Medical PG Practice Questions and MCQs

Question 381: What is the immediate energy source for muscle contraction?

A. ATP (Correct Answer)
B. GTP
C. Fatty acid
D. Creatine phosphate

Explanation: ***Correct Answer: ATP*** - **ATP (adenosine triphosphate)** is the direct and immediate source of energy for muscle contraction. The hydrolysis of ATP into **ADP (adenosine diphosphate)** and an inorganic phosphate molecule releases the energy required for the myosin head to detach from actin and reset for another power stroke. - While other molecules contribute to ATP regeneration, **ATP** itself is the molecule that directly powers the contractile proteins during the cross-bridge cycle. *Incorrect: GTP* - **GTP (guanosine triphosphate)** is an energy-carrying molecule similar to ATP, but it is primarily involved in **protein synthesis** and **signal transduction**, not direct muscle contraction. - Although it has high-energy phosphate bonds, muscle cells do not directly utilize **GTP** to power the cross-bridge cycle. *Incorrect: Fatty acid* - **Fatty acids** are a significant fuel source for endurance activities and long-term energy production, primarily through **beta-oxidation** and the **Krebs cycle** to generate large amounts of ATP. - However, fatty acids themselves are not the immediate energy source; they must first be metabolized to produce **ATP**, which then powers contraction. *Incorrect: Creatine phosphate* - **Creatine phosphate** acts as a rapid **reserve** for regenerating ATP, especially during the initial seconds of intense muscular activity through the creatine kinase reaction. - It donates a phosphate group to ADP to quickly form ATP, but it is not the molecule that directly causes muscle contraction. It *replenishes* ATP rather than directly powering the myosin-actin interaction.

Question 382: Noradrenaline is the major neurotransmitter in?

A. Postganglionic parasympathetic fibres
B. Autonomic ganglia
C. Preganglionic autonomic fibres
D. Postganglionic sympathetic fibers, except in sweat glands (Correct Answer)

Explanation: **Postganglionic sympathetic fibers, except in sweat glands** - **Noradrenaline** (norepinephrine) is the primary neurotransmitter released by most **postganglionic sympathetic nerve fibers**. - An important exception is the **sweat glands**, where postganglionic sympathetic fibers release **acetylcholine**. *Postganglionic parasympathetic fibres* - **Acetylcholine** is the major neurotransmitter released by all **postganglionic parasympathetic fibers**. - These fibers are part of the "rest and digest" system, mediating responses like reduced heart rate and increased digestive activity. *Autonomic ganglia* - **Acetylcholine** is the neurotransmitter released by both sympathetic and parasympathetic **preganglionic neurons** onto nicotinic receptors in the autonomic ganglia. - These ganglia act as relay stations, where preganglionic neurons synapse with postganglionic neurons. *Preganglionic autonomic fibres* - All **preganglionic sympathetic** and **preganglionic parasympathetic fibers** release **acetylcholine** as their neurotransmitter. - These fibers originate in the central nervous system and synapse in autonomic ganglia.

Question 383: Which reflex is primarily associated with the S1 segment?

A. Knee jerk
B. Calcaneal reflex (Correct Answer)
C. Anal reflex
D. None of the options

Explanation: ***Calcaneal reflex*** - The **calcaneal reflex**, also known as the **Achilles reflex**, primarily assesses the integrity of the **S1 nerve segment** (with minor S2 contribution). - A positive reflex indicates the functioning of the **gastrocnemius-soleus complex** and their innervating spinal roots via the tibial nerve. - This is a deep tendon reflex elicited by tapping the Achilles tendon, resulting in plantar flexion of the foot. *Knee jerk* - The **knee jerk** (patellar reflex) primarily assesses the **L3 and L4 spinal nerve segments** (with L2 contribution). - It involves the **quadriceps femoris muscle** and its innervation through the femoral nerve. - This reflex does not involve the S1 segment. *Anal reflex* - The **anal reflex** primarily assesses the integrity of the **S3, S4, and S5 spinal nerve segments**. - It involves the reflexive contraction of the **external anal sphincter** upon perianal stimulation. - S1 is not involved in this reflex arc. *None of the options* - This option is incorrect because the **calcaneal reflex (Achilles reflex)** is directly and primarily associated with the **S1 nerve segment**. - There is a clear correct answer among the given choices.

Question 384: Sharp pain is transmitted by which type of fibres?

A. Aα
B. Aβ
C. Aδ (Correct Answer)
D. C

Explanation: ***Aδ*** - **Aδ fibers** are **myelinated, medium-diameter afferent fibers** that conduct fast, sharp, localized pain. - They are responsible for the **initial, rapid sensation of acute pain**, allowing for quick withdrawal reflexes. *Aα* - **Aα fibers** are the **largest diameter, heavily myelinated fibers** responsible for proprioception and motor control, not pain transmission. - They have the **highest conduction velocity** among all nerve fibers. *Aβ* - **Aβ fibers** are **myelinated fibers** that primarily transmit touch, pressure, and vibration sensations, not pain. - They are involved in the **gate control theory of pain**, where their activation can inhibit pain signals from C and Aδ fibers. *C* - **C fibers** are **unmyelinated, small-diameter fibers** that transmit slow, dull, burning, and poorly localized pain. - They are responsible for the **delayed, persistent, and aching component of pain**.

Question 385: A 35-year-old female experiences a tingling sensation in her arm after watching TV for long hours with her hands under her head. Which type of nerve fibers is most likely to be affected due to this position?

A. B - fibers (autonomic)
B. C - fibers (pain and temperature)
C. Sympathetic nerve fibers
D. A-beta (Aβ) sensory nerve fibers (Correct Answer)

Explanation: ***A-beta (Aβ) sensory nerve fibers*** - The tingling sensation (paresthesia) described is a classic symptom of **A-beta fiber compression**. - **A-beta fibers** are large, myelinated sensory fibers that transmit light touch, pressure, vibration, and proprioception. - These fibers are **most susceptible to mechanical compression** due to their position and structure. - Positioning the hands under the head for extended periods compresses superficial nerves, causing temporary A-beta fiber dysfunction, which manifests as the characteristic "pins and needles" sensation. *B-fibers (autonomic)* - **B-fibers** are preganglionic autonomic fibers that mediate visceral functions, such as organ control and glandular secretions. - Compression of these fibers would lead to symptoms related to autonomic dysfunction (e.g., changes in sweating, blood pressure), not a tingling sensation in the arm. *C-fibers (pain and temperature)* - **C-fibers** are unmyelinated fibers that transmit slow, dull, aching pain and contribute to temperature sensation. - They are **less susceptible to compression** than larger myelinated fibers. - The primary sensation described (tingling/paresthesia) is characteristic of large myelinated fiber (A-beta) dysfunction, not C-fiber involvement. *Sympathetic nerve fibers* - **Sympathetic nerve fibers** regulate involuntary functions like heart rate, blood pressure, and sweating. - Their compression would cause symptoms such as changes in skin temperature, altered sweating, or blood vessel constriction (Horner's syndrome if severe), not a tingling sensation.

Question 386: In multiple sclerosis, slow conduction of motor and sensory pathways is due to?

A. Loss of myelin sheath (Correct Answer)
B. Dysfunction of sodium channels
C. Dysfunction of calcium channels
D. Defect in the nodes of Ranvier

Explanation: ***Loss of myelin sheath*** - Multiple sclerosis (MS) is characterized by **demyelination**, which is the destruction of the **myelin sheath** surrounding nerve fibers in the central nervous system. - Myelin acts as an electrical insulator, facilitating rapid, **saltatory conduction** of nerve impulses; its loss directly leads to **slowed or blocked signal transmission**. *Dysfunction of sodium channels* - While sodium channel dysfunction can occur secondary to demyelination, it is not the primary cause of slow conduction in MS but rather a downstream effect or an adaptive change. - The initial and fundamental problem leading to slowed conduction in MS is the **loss of the myelin sheath**, which renders the exposed axon less efficient at propagating action potentials. *Dysfunction of calcium channels* - Dysfunction of calcium channels is not the primary pathological mechanism responsible for the slowed conduction in MS. - While calcium dysregulation can play a role in **axonal damage** and neurodegeneration in MS, it is not the direct cause of the characteristic **slowed nerve impulse propagation**. *Defect in the nodes of Ranvier* - The **nodes of Ranvier** are uncovered gaps in the myelin sheath that are crucial for **saltatory conduction**. While their integrity is important, a primary "defect" in the nodes themselves is not the initial cause of slowed conduction in MS. - Slowed conduction occurs because the **myelin surrounding the axons** is lost, leading to longer distances for the action potential to travel and exposing segments of the axon unprepared for continuous conduction.

Question 387: Which muscle group is first affected by rigor mortis?

A. Jaw (Correct Answer)
B. Neck
C. Myocardium
D. Eyelids

Explanation: ***Jaw*** - Rigor mortis typically **first affects the jaw muscles** (masseter and temporalis) within **2-4 hours** after death. - This follows **Nysten's Law**, which describes the cephalocaudal progression of rigor mortis from smaller to larger muscles and from head to feet. - The **jaw muscles** are consistently documented in forensic medicine as the **initial site** of rigor mortis development. - Clinical significance: Jaw stiffness is an important early indicator for estimating post-mortem interval. *Eyelids* - While the eyelid muscles are small and fine, they are **not the first** muscle group to develop rigor mortis. - Eyelid muscles may show early changes, but the **jaw muscles precede them** in the classic progression. - The misconception arises from their small size, but anatomical location and usage patterns favor jaw muscle priority. *Neck* - Neck muscles are affected **early in the progression** of rigor mortis, typically following the jaw. - They are part of the cephalocaudal spread pattern, occurring within **2-6 hours** post-mortem. - However, they are **secondary** to the jaw muscles in the temporal sequence. *Myocardium* - The heart muscle undergoes rigor mortis but is **not among the first** muscle groups affected. - **Cardiac rigor** occurs as part of the generalized progression but after facial and neck muscles. - It may be important for forensic examination but does not represent the initial site of rigor mortis.

Question 388: What is the primary function of the Golgi tendon organ?

A. Sensing muscle tension (Correct Answer)
B. Sensing muscle length
C. Sensing proprioceptive information
D. Sensing pressure changes

Explanation: ***Sensing muscle tension*** - The **Golgi tendon organ (GTO)** is a **proprioceptor** located at the junction of a muscle and its tendon. - Its primary role is to monitor and protect the muscle from excessive **force** or **tension** during contraction. *Sensing muscle length* - This function is primarily attributed to **muscle spindles**, which are stretch receptors embedded within the muscle belly. - Muscle spindles detect changes in the **length** and **rate of change of length** of muscles. *Sensing proprioceptive information* - While the Golgi tendon organ is a **type of proprioceptor**, this option is too broad as proprioception encompasses sensing limb position and movement from multiple sources, including muscle spindles and joint receptors. - The GTO's specific role within proprioception is detecting **muscle tension**. *Sensing pressure changes* - **Pressure changes** are typically detected by various **mechanoreceptors** in the skin and deeper tissues (e.g., Pacinian corpuscles, Merkel cells), not primarily by the Golgi tendon organ. - The GTO is specifically tuned to the mechanical forces within the **tendon**.

Question 389: Locking of the knee involves which of the following?

A. Internal rotation of the tibia with the foot on the ground
B. Contraction of the popliteus muscle
C. Internal rotation of the femur with the foot on the ground (Correct Answer)
D. External rotation of femur with the foot off the ground

Explanation: ***Internal rotation of the femur with the foot on the ground*** - When the foot is on the ground (closed kinematic chain), the **femur rotates internally on the tibia** during the end stages of knee extension. This creates a more stable, "locked" position of the knee. - This **terminal rotation of the femur** increases the contact area and tension in the cruciate ligaments, enhancing joint stability for weight-bearing. *Internal rotation of the tibia with the foot on the ground* - This describes the action of the **popliteus muscle** when "unlocking" the knee from full extension, not the locking mechanism itself. - With the foot on the ground, the tibia is fixed, and internal rotation would typically be a movement for unlocking, not locking. *Contraction of the popliteus muscle* - The **popliteus muscle** is primarily responsible for **unlocking the knee** from full extension, by causing internal rotation of the tibia (or external rotation of the femur). - Its contraction would lead to initial flexion of the knee, releasing the locked position, not establishing it. *External rotation of femur with the foot off the ground* - With the foot off the ground (open kinematic chain), **external rotation of the tibia** occurs during the final degrees of extension to lock the knee, not external rotation of the femur. - The locking mechanism requires specific relative rotation between femur and tibia; external rotation of the femur alone would not achieve the screw-home mechanism necessary for knee locking.

Question 390: EPSP is due to?

A. Sodium ion influx (Correct Answer)
B. Potassium ion influx
C. Sodium ion efflux
D. Calcium ion influx

Explanation: ***Sodium ion influx*** - An **Excitatory Postsynaptic Potential (EPSP)** is caused primarily by the binding of an **excitatory neurotransmitter** to its receptor, leading to the opening of **ligand-gated ion channels** permeable to sodium (Na+) ions. - The **influx of positively charged sodium ions** into the postsynaptic neuron causes a **depolarization** of the membrane potential, making it more likely to reach the threshold for an action potential. *Potassium ion influx* - **Potassium (K+) influx** is not the primary mechanism for generating an EPSP; instead, **potassium efflux** (movement out of the cell) is typically involved in **repolarization** after an action potential or in generating **Inhibitory Postsynaptic Potentials (IPSPs)**. - The movement of K+ into the cell would make the membrane potential more negative, leading to **hyperpolarization** or preventing depolarization. *Sodium ion efflux* - **Sodium (Na+) efflux** is mediated by the **Na+/K+ pump** and is crucial for maintaining the resting membrane potential, but it does **not directly cause an EPSP**. - Pumping Na+ out of the cell would **hyperpolarize** the cell or oppose depolarization, making an action potential less likely. *Calcium ion influx* - While **calcium (Ca2+) influx** is vital for many neuronal processes, including **neurotransmitter release** from the presynaptic terminal, it is **not the primary ionic basis** for generating an EPSP in the postsynaptic neuron itself. - Significant Ca2+ influx can occur during an **action potential** or lead to intracellular signaling, but it's not the main depolarizing current responsible for an EPSP.

Practice by Chapter

Resting Membrane Potential

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Action Potential Generation and Propagation

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Neuromuscular Junction

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Skeletal Muscle Contraction

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Smooth Muscle Physiology

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Cardiac Muscle Properties

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Muscle Metabolism and Fatigue

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Motor Unit Function

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Neurotransmitters and Receptors

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Electrophysiological Measurements

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