Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology Indian Medical PG Practice Questions and MCQs

Question 111: Which of the following is associated with the 'All-or-none' law?

A. Action potential (Correct Answer)
B. Resting potential
C. Membrane potential
D. None of the above

Explanation: ### Explanation **1. Why Action Potential is Correct:** The **All-or-None Law** states that if a stimulus is strong enough to reach the **threshold potential** (usually -55mV), an action potential of constant magnitude and shape will be generated. If the stimulus is sub-threshold, no action potential occurs at all. Once triggered, the amplitude and velocity of the action potential remain independent of the strength of the stimulus. Therefore, the cell either "fires" completely or not at all. **2. Why Other Options are Incorrect:** * **Resting Membrane Potential (RMP):** This is the static electrical potential across a cell membrane when the cell is not excited (typically -70mV to -90mV). It is maintained by ion pumps and leak channels and does not follow the all-or-none principle; it can fluctuate slightly based on metabolic conditions. * **Membrane Potential:** This is a general term for the voltage difference across a membrane at any given time. It includes graded potentials (like EPSPs or IPSPs), which are **proportional** to the stimulus intensity and do not follow the all-or-none law. **3. High-Yield Clinical Pearls for NEET-PG:** * **Graded Potentials:** Unlike action potentials, local potentials (e.g., end-plate potentials, receptor potentials) are **not** all-or-none; they are proportional to stimulus strength and can be summated. * **Refractory Period:** The absolute refractory period ensures that action potentials are discrete events, preventing them from merging. * **Exceptions:** While a single nerve fiber follows the all-or-none law, a **whole nerve trunk** (composed of many fibers) does not, as it shows "graded" responses due to the recruitment of different fibers with varying thresholds.

Question 112: Action potential is transmitted in myofibrils via which structure?

A. Terminal cisterns
B. T-Tubules (Correct Answer)
C. Longitudinal tubules
D. Sarcomere

Explanation: **Explanation:** The transmission of an action potential from the sarcolemma (cell membrane) into the interior of a muscle fiber is mediated by the **T-tubules (Transverse tubules)**. **1. Why T-Tubules are correct:** T-tubules are deep invaginations of the sarcolemma that run perpendicular to the myofibrils. When an action potential spreads across the muscle surface, it travels down the T-tubules to reach the deep-seated sarcoplasmic reticulum. This triggers the **Dihydropyridine (DHP) receptors** in the T-tubule membrane, which are mechanically coupled to **Ryanodine receptors (RyR)** on the sarcoplasmic reticulum, leading to calcium release and muscle contraction. This process is known as **Excitation-Contraction Coupling**. **2. Why other options are incorrect:** * **Terminal cisterns:** These are enlarged areas of the sarcoplasmic reticulum that *store* calcium. While they release calcium upon stimulation, they do not transmit the action potential itself. * **Longitudinal tubules:** These are the central portions of the sarcoplasmic reticulum primarily involved in calcium reuptake via SERCA pumps, not the initial transmission of the electrical impulse. * **Sarcomere:** This is the basic structural and functional unit of a myofibril (between two Z-lines). It is the site of contraction, not the conduit for the action potential. **High-Yield Clinical Pearls for NEET-PG:** * **The Triad:** In skeletal muscle, a triad consists of one T-tubule and two flanking terminal cisternae, typically located at the **A-I junction**. (In cardiac muscle, it is a *dyad* located at the Z-line). * **Malignant Hyperthermia:** Caused by a mutation in the **Ryanodine receptor (RyR1)**, leading to excessive calcium release when exposed to volatile anesthetics (e.g., Halothane). * **L-type Calcium Channels:** The DHP receptors in T-tubules act as voltage sensors in skeletal muscle but function as actual calcium channels in cardiac muscle.

Question 113: What happens to muscle during rigor mortis?

A. Stiffens
B. Shortens
C. Stiffens and shortens (Correct Answer)
D. Stiffens and lengthens

Explanation: **Explanation:** Rigor mortis is the post-mortem state of muscle rigidity caused by the depletion of **Adenosine Triphosphate (ATP)**. **1. Why "Stiffens and Shortens" is correct:** * **Stiffening:** In a living muscle, ATP is required to break the cross-bridge between actin and myosin filaments. After death, ATP production ceases. Without ATP, the myosin heads remain permanently attached to actin in a "locked" position, leading to extreme rigidity (stiffness). * **Shortening:** Shortly after death, the sarcoplasmic reticulum membranes lose integrity, leaking **Calcium ions** into the sarcoplasm. This calcium binds to Troponin C, triggering the power stroke. Since there is no ATP to sequester calcium back or detach the myosin heads, the muscle fibers contract and remain in a shortened state. **2. Analysis of Incorrect Options:** * **A (Stiffens only):** While stiffness is the most prominent feature, it ignores the physiological contraction (shortening) caused by the initial calcium release. * **B (Shortens only):** This is incomplete as it fails to account for the permanent cross-bridge formation that results in the characteristic "rigor" or stiffness. * **D (Stiffens and lengthens):** Lengthening is physiologically impossible during rigor because the sliding filament mechanism pulls the Z-lines closer together during the final calcium-mediated contraction. **Clinical Pearls for NEET-PG:** * **Timeline:** Rigor mortis typically starts **2–6 hours** after death, becomes maximal at **12 hours**, and disappears after **36–48 hours** due to muscle autolysis (proteolysis of myosin heads). * **Sequence:** It follows **Nysten’s Law**, appearing first in involuntary muscles (heart), then small voluntary muscles (eyelids, jaw), and finally spreading craniocaudally to the limbs. * **ATP Role:** Remember, ATP is needed for both **contraction** (via myosin ATPase) and **relaxation** (to break the cross-bridge). Rigor is a failure of relaxation.

Question 114: What is saltatory conduction?

A. Conduction from a presynaptic to a postsynaptic neuron.
B. Conduction within the muscles of the T-tubule system.
C. The jumping of depolarization from node to node in myelinated axons. (Correct Answer)
D. Conduction of an impulse in both directions along an axon.

Explanation: **Explanation:** **Saltatory conduction** (from the Latin *saltare*, meaning "to leap") is the process by which nerve impulses are transmitted along **myelinated axons**. Myelin acts as an electrical insulator, preventing ion flow across the axonal membrane. Consequently, action potentials cannot occur in myelinated segments; instead, depolarization "jumps" between the **Nodes of Ranvier**—uninsulated gaps where voltage-gated sodium channels are highly concentrated. This mechanism significantly increases conduction velocity and conserves metabolic energy (ATP), as the Na⁺-K⁺ pump only needs to restore gradients at the nodes. **Analysis of Incorrect Options:** * **Option A:** Describes **synaptic transmission**, the chemical or electrical communication between two distinct neurons. * **Option B:** Refers to the **excitation-contraction coupling** mechanism, where action potentials travel down T-tubules to trigger calcium release from the sarcoplasmic reticulum. * **Option D:** Describes **bidirectional conduction**. While experimental stimulation can cause impulses to travel both ways, physiological conduction is typically **orthodromic** (one direction). **High-Yield Clinical Pearls for NEET-PG:** * **Demyelinating Diseases:** In conditions like **Multiple Sclerosis** (CNS) and **Guillain-Barré Syndrome** (PNS), loss of myelin disrupts saltatory conduction, leading to "conduction block" or slowed signal transmission. * **Velocity:** Conduction velocity in myelinated fibers is directly proportional to the fiber diameter ($V \propto \text{diameter}$), whereas in unmyelinated fibers, it is proportional to the square root of the diameter ($V \propto \sqrt{\text{diameter}}$). * **Energy Efficiency:** Saltatory conduction is nearly 100 times more energy-efficient than continuous conduction.

Question 115: What is the first change that occurs in a cut nerve?

A. Schwann cell proliferation
B. Degeneration of the myelin sheath (Correct Answer)
C. Chromatolysis
D. Degeneration of the neurilemma

Explanation: When a peripheral nerve is transected, it undergoes a series of stereotypical changes known as **Wallerian Degeneration**. ### Explanation of the Correct Answer The correct answer is **B. Degeneration of the myelin sheath**. Wallerian degeneration refers to the process that occurs in the distal segment of a cut nerve. The very first morphological change, occurring within the first **24–48 hours**, is the fragmentation of the axon and the simultaneous **breakdown of the myelin sheath** into droplets (ellipsoids). This occurs because the distal segment is separated from the neuronal cell body, which provides the essential proteins and lipids required for axonal and myelin maintenance. ### Why Other Options are Incorrect * **A. Schwann cell proliferation:** This occurs slightly later (starting around day 3–4). Schwann cells proliferate to form **Bungner bands**, which act as a scaffold to guide regenerating axons. * **C. Chromatolysis:** This is a change seen in the **cell body (soma)**, not the cut nerve fiber itself. It involves the swelling of the cell body and the disappearance of Nissl granules. It typically peaks between 1–3 weeks. * **D. Degeneration of the neurilemma:** The neurilemma (the outermost nucleated cytoplasmic layer of Schwann cells) does **not** degenerate; instead, it remains intact to provide the tube through which the nerve eventually regenerates. ### High-Yield NEET-PG Pearls * **Wallerian Degeneration:** Occurs in the **distal segment** (from the site of injury to the nerve terminal). * **Retrograde Degeneration:** Occurs in the **proximal segment** (up to the first Node of Ranvier). * **Nissl Granules:** Composed of Rough Endoplasmic Reticulum (RER); their disappearance during chromatolysis indicates active protein synthesis for repair. * **Rate of Regeneration:** Peripheral nerves typically regenerate at a rate of **1–3 mm/day**. * **Blood-Brain Barrier:** In the CNS, Wallerian degeneration is much slower because oligodendrocytes do not facilitate regeneration like Schwann cells do.

Question 116: Skeletal muscle contraction ends when:

A. Ions move out of the cytoplasm
B. Acetylcholine is absorbed from the neuromuscular junction
C. Receptors close and are drawn inward
D. Calcium levels decrease outside the sarcoplasmic reticulum (Correct Answer)

Explanation: ### Explanation **1. Why Option D is Correct:** Skeletal muscle contraction is a calcium-dependent process. For relaxation (the end of contraction) to occur, the concentration of free cytosolic calcium must decrease. This is achieved by the **SERCA pump** (Sarcoplasmic/Endoplasmic Reticulum Calcium ATPase), which actively transports calcium ions from the sarcoplasm (outside the SR) back into the **Sarcoplasmic Reticulum (SR)** against a concentration gradient. As calcium levels outside the SR drop, calcium dissociates from **Troponin C**, allowing the troponin-tropomyosin complex to re-mask the active sites on actin, preventing further cross-bridge cycling. **2. Why Other Options are Incorrect:** * **Option A:** While ions (like $K^+$) move out of the cytoplasm during repolarization, this restores the membrane potential but does not directly terminate the mechanical contraction; only the removal of $Ca^{2+}$ stops the actin-myosin interaction. * **Option B:** Acetylcholine (ACh) is not "absorbed"; it is **hydrolyzed** by the enzyme Acetylcholinesterase (AChE) into choline and acetate. * **Option C:** While receptors undergo desensitization or internalisation over long periods, this is not the physiological mechanism for ending a single muscle twitch. **3. High-Yield Clinical Pearls for NEET-PG:** * **Calsequestrin:** A protein inside the SR that binds to $Ca^{2+}$, allowing the SR to store large amounts of calcium at low osmotic pressure. * **Rigor Mortis:** Occurs because ATP is required for the SERCA pump to sequester calcium and for the myosin head to detach from actin. Without ATP, $Ca^{2+}$ remains high and cross-bridges stay locked. * **Malignant Hyperthermia:** Caused by a mutation in the **Ryanodine Receptor (RyR)**, leading to excessive calcium release and sustained muscle contraction/heat production. * **Phospholamban:** A protein that regulates the SERCA pump (primarily in cardiac muscle); when dephosphorylated, it inhibits $Ca^{2+}$ reuptake.

Question 117: All of the following are true regarding the Golgi tendon organ, EXCEPT:

A. Mediates the inverse stretch reflex
B. Detects changes in muscle length (Correct Answer)
C. Inhibits the alpha motor neuron
D. Is an encapsulated sensory receptor

Explanation: ### Explanation The **Golgi Tendon Organ (GTO)** is a specialized sensory receptor located at the junction of muscle fibers and tendons. Its primary function is to monitor **muscle tension** rather than length. **Why Option B is the Correct Answer (The Exception):** The GTO is arranged **in series** with muscle fibers. When a muscle contracts, it pulls on the tendon, activating the GTO. It is highly sensitive to changes in **tension/force**. In contrast, the **Muscle Spindle** is arranged in parallel and is the receptor responsible for detecting changes in **muscle length** and the rate of change in length. **Analysis of Other Options:** * **Option A & C:** The GTO mediates the **Inverse Stretch Reflex** (Autogenic Inhibition). When excessive tension is detected, the GTO sends impulses via **Ib afferent fibers** to the spinal cord. These synapse with inhibitory interneurons that **inhibit the alpha motor neuron** of the same muscle, causing it to relax. This serves as a protective mechanism to prevent tendon avulsion or muscle tearing. * **Option D:** The GTO is indeed an **encapsulated sensory receptor** consisting of a network of collagen fibers enclosed in a capsule. **High-Yield Facts for NEET-PG:** * **Muscle Spindle:** Detects **Length**; Afferents: **Ia** (primary) and **II** (secondary); Reflex: **Stretch Reflex** (monosynaptic). * **Golgi Tendon Organ:** Detects **Tension**; Afferents: **Ib**; Reflex: **Inverse Stretch Reflex** (polysynaptic). * **Clasp-Knife Phenomenon:** This clinical sign (seen in UMN lesions) is attributed to the activation of the inverse stretch reflex mediated by GTOs when a spastic muscle is forcefully stretched.

Question 118: After-hyperpolarization during nerve conduction is due to:

A. Slow entry of Na+
B. Pumping of Na+ outside
C. Slow entry of K+ (Correct Answer)
D. Pumping of K+ outside

Explanation: ### Explanation **1. Why "Slow entry of K+" is correct:** After-hyperpolarization (AHP) occurs at the end of an action potential when the membrane potential becomes more negative than the resting membrane potential (RMP). This is primarily due to the **prolonged opening of voltage-gated K+ channels**. While Na+ channels close rapidly (inactivation), K+ channels are "slow" to close. Even after the RMP is reached during repolarization, K+ continues to exit the cell down its electrochemical gradient. This continued efflux brings the membrane potential closer to the **Equilibrium Potential of Potassium (-94 mV)**, which is more negative than the RMP (-70 mV). *Note: In the context of this question, "Slow entry of K+" refers to the delayed kinetics of the K+ channels remaining open, allowing K+ to move towards its equilibrium.* **2. Why the other options are incorrect:** * **Option A (Slow entry of Na+):** Na+ entry causes depolarization (making the cell more positive), which is the opposite of hyperpolarization. * **Option B (Pumping of Na+ outside):** The Na+-K+ ATPase pump is electrogenic but works continuously to maintain gradients; it is not the primary cause of the rapid voltage changes seen in AHP. * **Option D (Pumping of K+ outside):** K+ moves out through **passive channels** (diffusion) during AHP, not via active "pumping" mechanisms. **3. High-Yield Facts for NEET-PG:** * **Depolarization:** Due to Na+ influx (opening of voltage-gated Na+ channels). * **Repolarization:** Due to K+ efflux (opening of voltage-gated K+ channels). * **Absolute Refractory Period:** Corresponds to the period from the threshold to the early part of repolarization (Na+ channels are inactivated). * **Relative Refractory Period:** Corresponds to the period of After-hyperpolarization. * **Tetrodotoxin (TTX):** Blocks voltage-gated Na+ channels. * **Tetraethylammonium (TEA):** Blocks voltage-gated K+ channels, thereby abolishing after-hyperpolarization.

Question 119: Following traumatic peripheral nerve transection, re-growth usually occurs at which of the following rates?

A. 0.1 mm per day
B. 1 mm per day (Correct Answer)
C. 5 mm per day
D. 1 cm per day

Explanation: **Explanation:** The correct answer is **1 mm per day (Option B)**. Following a peripheral nerve injury (transection), the distal segment undergoes **Wallerian degeneration**, while the proximal segment undergoes **regeneration**. Once the axonal sprouts cross the lesion site and enter the distal endoneurial tubes, they grow toward the target organ. This regenerative process is driven by slow axonal transport and typically occurs at a rate of **1 mm/day** (or approximately 1 inch per month). **Analysis of Incorrect Options:** * **Option A (0.1 mm/day):** This rate is too slow. While initial "die-back" and the latent period before sprouting may delay visible progress, the actual growth rate is significantly higher. * **Option C (5 mm/day):** This is an overestimation. While some experimental conditions or very young patients might show slightly faster rates, the standard physiological average used in clinical practice is 1 mm/day. * **Option D (1 cm/day):** This is physiologically impossible for human nerve regeneration. Such a rapid rate would lead to recovery in days for injuries that typically take months. **High-Yield Facts for NEET-PG:** * **Hoffmann-Tinel Sign:** A clinical test where distal percussion over the regenerating nerve elicits a tingling sensation. The distal-most point of tingling indicates the extent of axonal regrowth, allowing clinicians to track the 1 mm/day progress. * **Factors affecting regeneration:** Regeneration is faster in **crush injuries** (Sunderland Grade 2) than in complete transections because the endoneurial sheath remains intact to guide the axons. * **Proximal vs. Distal:** Regeneration is generally faster in proximal segments compared to distal segments. * **CNS vs. PNS:** Regeneration occurs in the PNS (aided by Schwann cells) but is virtually absent in the CNS due to inhibitory factors like Nogo-A and the absence of a basement membrane.

Question 120: Which nerve fiber is most commonly affected by pressure?

A. Aa
B. AP (Correct Answer)
C. Ay
D. C

Explanation: **Explanation:** The susceptibility of nerve fibers to different types of insults depends on their physiological characteristics, such as diameter and myelination. The correct answer is **Aβ (Type A beta)**, as it belongs to the group of thick, myelinated fibers that are most sensitive to mechanical compression. **Why Aβ is correct:** According to **Erlanger and Gasser’s classification**, nerve fibers show varying sensitivity to pressure, hypoxia, and local anesthetics. * **Pressure:** Large-diameter, heavily myelinated fibers are the most sensitive. Among the options, **Aβ** (involved in touch and pressure sensation) is a large myelinated fiber. When pressure is applied (e.g., a limb "falling asleep"), these fibers are the first to lose conduction. * The order of sensitivity to pressure is: **Type A > Type B > Type C.** **Why other options are incorrect:** * **Aα (Alpha):** While these are the largest fibers (motor and proprioception), Aβ is traditionally cited in clinical exams as the representative fiber for pressure-induced block (paresthesia). However, in a strict hierarchy, all Type A fibers are more sensitive than B or C. * **Aγ (Gamma):** These are medium-sized myelinated fibers supplying muscle spindles. They are less sensitive to pressure than the larger Aα and Aβ fibers. * **C fibers:** These are small, unmyelinated fibers carrying slow pain and temperature. They are the **least sensitive to pressure** but the **most sensitive to local anesthetics**. **High-Yield Clinical Pearls for NEET-PG:** To remember the sensitivity patterns, use the mnemonic **"PLA"**: 1. **P**ressure: **A** fibers (Most sensitive) > B > C 2. **L**ocal Anesthetic: **C** fibers (Most sensitive) > B > A 3. **A**noxia (Hypoxia): **B** fibers (Most sensitive) > A > C * **Clinical Correlation:** In "Saturday Night Palsy" (radial nerve compression), the large myelinated motor and sensory fibers are blocked first, while dull pain (C fibers) may still be perceived.

Practice by Chapter

Resting Membrane Potential

Practice Questions

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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