Nerve and Muscle Physiology — MCQs
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Fast muscle fibers are characterized by which of the following?
What is the relationship between nerve thickness and conduction velocity of myelinated nerves?
In tetany, what causes the increased membrane excitability?
TTX-resistant sodium channels are caused by the involvement of which of the following?
Tetrodotoxin blocks which of the following during the action potential?
The gamma efferent system is involved in which of the following?
The sodium gradient across the nerve cell membrane is:
What is true about tropomyosin?
Neuronal degeneration is seen in all of the following conditions except?
Maximum conduction occurs in which type of nerve fibers?
Nerve and Muscle Physiology Indian Medical PG Practice Questions and MCQs
Question 1: Fast muscle fibers are characterized by which of the following?
- A. Red appearance
- B. High oxidative capacity
- C. Tonic contraction
- D. High glycolytic capacity (Correct Answer)
Explanation: ### Explanation Skeletal muscle fibers are classified into two main types based on their metabolic profile and contraction speed: **Type I (Slow-twitch)** and **Type II (Fast-twitch)**. **Why the correct answer is right:** **Type II (Fast-twitch) fibers** are designed for rapid, powerful bursts of activity. To achieve this, they rely primarily on **anaerobic metabolism**. They possess high concentrations of **glycolytic enzymes** (like phosphorylase and LDH) and store significant amounts of glycogen. This allows them to generate ATP quickly through glycolysis, hence their **high glycolytic capacity**. **Why the incorrect options are wrong:** * **A. Red appearance:** This is a feature of **Type I fibers**. They contain high amounts of **myoglobin** (an iron-containing oxygen-binding protein), which gives them a deep red color. Type II fibers have low myoglobin and appear pale/white. * **B. High oxidative capacity:** This characterizes **Type I fibers**, which are packed with mitochondria and surrounded by dense capillary networks to support aerobic respiration. Type II fibers have fewer mitochondria and lower oxidative capacity. * **C. Tonic contraction:** Type I fibers are "tonic" or "antigravity" muscles (e.g., soleus) because they are fatigue-resistant and maintain posture. Type II fibers are "phasic," meaning they contract rapidly but fatigue quickly. ### High-Yield Clinical Pearls for NEET-PG * **Type I (Slow):** "One Slow Red Ox" (Type **I**, **Slow**-twitch, **Red** color, **Ox**idative metabolism). * **Type II (Fast):** Large diameter, high ATPase activity, and high sarcoplasmic reticulum development for rapid $Ca^{2+}$ release. * **Intermediate Fibers (Type IIa):** These are fast-twitch but have both oxidative and glycolytic capacities (Fast-Oxidative-Glycolytic). * **Muscle Examples:** The **Soleus** is predominantly Type I (postural), while the **Extraocular muscles** and gastrocnemius have a high proportion of Type II fibers for rapid movement.
Question 2: What is the relationship between nerve thickness and conduction velocity of myelinated nerves?
- A. Linear (Correct Answer)
- B. Parabolic
- C. Hyperbolic
- D. No relation
Explanation: **Explanation:** The relationship between the diameter of a myelinated nerve fiber and its conduction velocity is **linear**. According to the **Hursh transformation**, the conduction velocity (V) in meters per second is approximately 6 times the external diameter (D) in micrometers ($V \approx 6 \times D$). In myelinated nerves, conduction occurs via **saltatory conduction**. As the fiber diameter increases, internal axial resistance decreases significantly, and the distance between the Nodes of Ranvier (internodal length) increases. This allows the action potential to "jump" further and faster, resulting in a direct proportionality between thickness and speed. **Analysis of Options:** * **B. Parabolic & C. Hyperbolic:** These are incorrect because the increase in velocity does not follow a squared or inverse curve. While unmyelinated fibers show a relationship where velocity is proportional to the *square root* of the diameter (making it non-linear), myelinated fibers strictly follow a linear progression. * **D. No relation:** This is incorrect as fiber diameter is the primary anatomical determinant of conduction speed. **High-Yield Facts for NEET-PG:** * **Erlanger-Gasser Classification:** Type A fibers (thickest, myelinated) have the highest velocity, while Type C fibers (thinnest, unmyelinated) have the slowest. * **Myelination Effect:** Myelin increases conduction velocity by increasing membrane resistance and decreasing membrane capacitance. * **Clinical Correlation:** In demyelinating diseases like **Guillain-Barré Syndrome (GBS)** or **Multiple Sclerosis**, the loss of myelin disrupts this linear relationship, leading to significantly slowed conduction or conduction block.
Question 3: In tetany, what causes the increased membrane excitability?
- A. Decreased release of inhibitory neurotransmitter from nerve terminals
- B. Depolarization of the nerve and muscle membranes (Correct Answer)
- C. Spontaneous release of calcium from the sarcoplasmic reticulum
- D. Activation of sodium channels at more negative membrane potentials
Explanation: ### Explanation **1. Why the Correct Answer is Right:** Tetany is primarily caused by **hypocalcemia**. In the extracellular fluid (ECF), calcium ions ($Ca^{2+}$) normally exert a "stabilizing" effect on voltage-gated sodium channels. They do this by binding to the outer surface of the channel protein, increasing the local positive charge and maintaining a high threshold for activation. When ECF calcium levels drop, this stabilizing effect is lost. The resting membrane potential (RMP) effectively moves closer to the threshold potential, or more accurately, the **activation threshold of sodium channels shifts to a more negative value**. This results in a state of partial **depolarization of the nerve and muscle membranes**, making them hyper-excitable. Even minor stimuli can trigger repetitive action potentials, leading to involuntary muscle contractions (tetany). **2. Why the Other Options are Wrong:** * **Option A:** This describes the mechanism of **Tetanus** (caused by *Clostridium tetani* toxin), which inhibits GABA and glycine release. Tetany (hypocalcemia) is a metabolic/electrolyte derangement, not a loss of inhibition. * **Option C:** Spontaneous calcium release from the SR is associated with conditions like **Malignant Hyperthermia** (RyR1 mutation), not the extracellular electrolyte imbalance seen in tetany. * **Option D:** While sodium channels *are* activated more easily, the physiological hallmark of the membrane state in hypocalcemia is described as a functional **depolarization** (reduction in the potential difference across the membrane). **3. High-Yield Clinical Pearls for NEET-PG:** * **Trousseau’s Sign:** Carpal spasm induced by inflating a BP cuff above systolic pressure (more sensitive than Chvostek's). * **Chvostek’s Sign:** Tapping the facial nerve leads to twitching of facial muscles. * **Hypocalcemia ECG:** Characterized by **prolonged QT interval** (due to lengthened ST segment). * **Magnesium Connection:** Hypomagnesemia can cause refractory hypocalcemia because $Mg^{2+}$ is required for PTH secretion and action.
Question 4: TTX-resistant sodium channels are caused by the involvement of which of the following?
- A. Nav 1.1
- B. Nav 1.8 (Correct Answer)
- C. TRPI
- D. NMD4
Explanation: **Explanation:** The correct answer is **Nav 1.8**. Voltage-gated sodium channels ($Na_v$) are classified based on their sensitivity to **Tetrodotoxin (TTX)**, a potent neurotoxin derived from pufferfish that blocks the extracellular pore of the channel. 1. **Why Nav 1.8 is correct:** Most voltage-gated sodium channels (Nav 1.1–1.4, 1.6, 1.7) are **TTX-sensitive**, meaning they are inhibited by nanomolar concentrations of the toxin. However, **Nav 1.8** and **Nav 1.9** (primarily found in dorsal root ganglion nociceptors) and **Nav 1.5** (found in cardiac muscle) possess a structural variation—specifically a substitution of a cysteine or serine for phenylalanine/tyrosine at a critical binding site—making them **TTX-resistant**. Nav 1.8 plays a crucial role in the transmission of inflammatory and mechanical pain. 2. **Why other options are incorrect:** * **Nav 1.1:** This is a classic **TTX-sensitive** channel found primarily in the Central Nervous System (CNS). Mutations in this channel are associated with Dravet syndrome (epilepsy). * **TRPI (TRPV1):** This refers to Transient Receptor Potential channels. These are non-selective cation channels (not specific sodium channels) activated by heat and capsaicin. * **NMD4:** This appears to be a distractor. **NMDA** receptors are glutamate-gated ion channels involved in synaptic plasticity, not voltage-gated sodium channels. **High-Yield Facts for NEET-PG:** * **TTX-Resistant Channels:** Nav 1.5 (Heart), Nav 1.8, and Nav 1.9 (Nociceptors). * **Nav 1.5 Clinical Link:** It is the primary sodium channel in the heart; its resistance to TTX explains why pufferfish poisoning causes neurological symptoms and paralysis but often spares cardiac conduction until late stages. * **Mechanism of TTX:** It binds to the **P-loop** of the alpha subunit, physically plugging the channel pore.
Question 5: Tetrodotoxin blocks which of the following during the action potential?
- A. Na+ channels (Correct Answer)
- B. K+ channels
- C. Na+ channels during the resting state
- D. K+ channels during the resting state
Explanation: **Explanation:** **Mechanism of Action:** Tetrodotoxin (TTX) is a potent neurotoxin that specifically and reversibly binds to the extracellular pore of **voltage-gated Na+ channels**. By blocking these channels, it prevents the rapid influx of sodium ions required for the **depolarization phase** of the action potential. This leads to the failure of nerve impulse conduction and muscle paralysis. **Analysis of Options:** * **Option A (Correct):** TTX blocks voltage-gated Na+ channels, specifically inhibiting the upstroke of the action potential. * **Option B (Incorrect):** K+ channels are responsible for the repolarization phase. These are blocked by agents like **Tetraethylammonium (TEA)**, not TTX. * **Options C & D (Incorrect):** The resting membrane potential is primarily maintained by **K+ leak channels** and the Na+-K+ ATPase pump. TTX specifically targets the voltage-gated channels that open during an active impulse, rather than the channels responsible for the resting state. **High-Yield Clinical Pearls for NEET-PG:** 1. **Source:** TTX is found in the **Pufferfish (Fugu)**, blue-ringed octopus, and certain newts. 2. **Symptoms:** Ingestion leads to paresthesia, flaccid paralysis, and potentially fatal respiratory failure (due to diaphragm paralysis), while the patient remains conscious. 3. **Saxitoxin:** Produced by dinoflagellates (Red Tide), it has a similar mechanism of action to TTX (blocks Na+ channels). 4. **Batrachotoxin:** Found in poison dart frogs; unlike TTX, it keeps Na+ channels **permanently open**, causing persistent depolarization. 5. **Dendrotoxin:** A snake toxin (Mamba) that blocks voltage-gated **K+ channels**.
Question 6: The gamma efferent system is involved in which of the following?
- A. Tendon reflex
- B. Clonus
- C. Muscle tone
- D. All of the above (Correct Answer)
Explanation: The **gamma efferent system** consists of small motor neurons in the anterior horn of the spinal cord that innervate the **intrafusal muscle fibers** of the muscle spindle. Its primary role is to regulate the sensitivity of the spindle to stretch. ### Why "All of the Above" is Correct: The gamma system is the physiological basis for the **Gamma Loop**, which maintains muscle spindle sensitivity even during muscle contraction. 1. **Muscle Tone (Option C):** This is the fundamental function of the gamma system. By causing contraction of the ends of intrafusal fibers, gamma efferents stretch the central sensory portion of the spindle. This triggers alpha motor neurons via the stretch reflex, maintaining a continuous state of partial muscle contraction (basal muscle tone). 2. **Tendon Reflex (Option A):** Deep tendon reflexes (e.g., knee jerk) are monosynaptic stretch reflexes. The gamma system sets the "gain" or sensitivity of these reflexes. High gamma discharge leads to brisk reflexes, while low discharge results in sluggish reflexes. 3. **Clonus (Option B):** Clonus is a series of involuntary, rhythmic muscle contractions. It occurs due to a hyperactive stretch reflex, typically seen in upper motor neuron (UMN) lesions. This hyperactivity is driven by **gamma motor neuron overactivity**, which makes the spindles hypersensitive to even slight stretches. ### High-Yield NEET-PG Pearls: * **Alpha-Gamma Co-activation:** During voluntary movement, both alpha and gamma motor neurons fire simultaneously. This prevents the muscle spindle from going "slack" during contraction, allowing the brain to monitor muscle length continuously. * **Anxiety & Gamma Discharge:** Anxiety increases gamma efferent discharge, which is why anxious patients often exhibit hyperactive tendon reflexes. * **Jendrassik Maneuver:** This clinical technique increases gamma efferent activity, reinforcing reflexes that are otherwise difficult to elicit.
Question 7: The sodium gradient across the nerve cell membrane is:
- A. A result of the Donnan equilibrium
- B. Significantly changed during an action potential
- C. Used as a source of energy for the transport of other ions (Correct Answer)
- D. An important determinant of the resting membrane potential
Explanation: ### Explanation **Correct Answer: C. Used as a source of energy for the transport of other ions** The sodium (Na⁺) gradient is maintained by the primary active transport of the Na⁺-K⁺ ATPase pump, which keeps extracellular Na⁺ high and intracellular Na⁺ low. This steep concentration gradient represents **potential energy**. This energy is harnessed by **secondary active transporters** (cotransporters and exchangers) to move other substances against their own gradients. Examples include the **Na⁺-Glucose symporter (SGLT)** in the renal tubules and the **Na⁺-Ca²⁺ exchanger** in cardiac myocytes. **Why other options are incorrect:** * **Option A:** The Donnan equilibrium describes the behavior of charged particles near a semi-permeable membrane containing non-diffusible ions (like proteins). It does not create the Na⁺ gradient; in fact, the Na⁺-K⁺ pump actively works to counteract the osmotic imbalances that Donnan forces would otherwise create. * **Option B:** During an action potential, Na⁺ channels open and ions rush in, but the **actual number of ions** moving is minuscule compared to the total concentration. The bulk chemical gradient remains virtually unchanged. * **Option C:** The **Resting Membrane Potential (RMP)** is primarily determined by the **permeability of Potassium (K⁺)**, as the membrane is much more "leaky" to K⁺ than Na⁺ at rest. Na⁺ permeability contributes only minimally to the RMP. **High-Yield Clinical Pearls for NEET-PG:** * **RMP of a typical nerve fiber:** -70 mV (primarily due to K⁺ efflux). * **Equilibrium Potential:** Calculated using the **Nernst Equation**. For Na⁺, it is approximately +60 mV; for K⁺, it is -90 mV. * **Digitalis Mechanism:** Inhibits the Na⁺-K⁺ ATPase, which decreases the Na⁺ gradient. This subsequently slows the Na⁺-Ca²⁺ exchanger, increasing intracellular Ca²⁺ and improving cardiac contractility.
Question 8: What is true about tropomyosin?
- A. Lies on top of troponin
- B. Lies on top of actin (Correct Answer)
- C. ATP binds to it
- D. Calcium binds to it
Explanation: **Explanation:** **1. Why the Correct Answer is Right:** Tropomyosin is a long, rod-shaped protein that consists of two polypeptide chains coiled around each other. In a resting muscle fiber, tropomyosin molecules lie in the **grooves of the actin filament**, physically covering the active sites (myosin-binding sites) on the actin molecules. This prevents the interaction between actin and myosin heads, thereby maintaining the muscle in a relaxed state. **2. Why the Other Options are Incorrect:** * **Option A:** Tropomyosin does not lie on top of troponin. Instead, the **Troponin complex** (consisting of subunits T, I, and C) sits at regular intervals *on top* of the tropomyosin molecule. Troponin T specifically functions to bind the troponin complex to tropomyosin. * **Option C:** ATP does not bind to tropomyosin. ATP binds to the **Myosin head** (specifically at the ATPase site) to provide the energy required for the power stroke and to facilitate the detachment of the cross-bridge. * **Option D:** Calcium does not bind to tropomyosin. Calcium binds to **Troponin C**. This binding causes a conformational change in the troponin-tropomyosin complex, pulling tropomyosin away from the active sites on actin to initiate contraction. **High-Yield NEET-PG Pearls:** * **Regulatory Proteins:** Tropomyosin and Troponin are known as regulatory proteins, while Actin and Myosin are contractile proteins. * **The "Lock":** Think of tropomyosin as the "safety lock" on actin. * **Length:** One tropomyosin molecule covers approximately **seven G-actin residues**. * **Clinical Correlation:** Mutations in the genes encoding tropomyosin (TPM1) or troponin are common causes of **Familial Hypertrophic Cardiomyopathy (HCM)**.
Question 9: Neuronal degeneration is seen in all of the following conditions except?
- A. Crush nerve injury
- B. Fetal development
- C. Senescence
- D. Neuropraxia (Correct Answer)
Explanation: **Explanation:** The correct answer is **Neuropraxia** because it is the mildest form of nerve injury (Seddon’s Classification) characterized by a temporary physiological conduction block without any structural damage to the axon or the connective tissue sheath. Since the axon remains intact, **Wallerian degeneration does not occur**, and recovery is typically complete within days to weeks once the pressure is relieved. **Analysis of Options:** * **Crush Nerve Injury (Axonotmesis):** In a crush injury, the axon is physically disrupted. This triggers Wallerian degeneration of the distal segment. While the endoneurial sheath remains intact to guide regeneration, neuronal degeneration is a hallmark of the initial pathology. * **Fetal Development:** Programmed cell death (**Apoptosis**) is a physiological process during neurodevelopment. Excess neurons are produced, and those that fail to establish functional synaptic connections undergo degeneration to refine the neural network. * **Senescence:** Normal aging is associated with progressive neuronal loss, cortical thinning, and a decrease in neurotransmitter levels. This is a form of chronic, physiological neuronal degeneration. **High-Yield Pearls for NEET-PG:** * **Seddon’s Classification:** 1. **Neuropraxia:** Conduction block; no degeneration; fast recovery. 2. **Axonotmesis:** Axon broken; sheath intact; Wallerian degeneration occurs; slow recovery (1mm/day). 3. **Neurotmesis:** Both axon and sheath are severed; requires surgical intervention. * **Wallerian Degeneration:** Occurs in the **distal** segment of a cut peripheral nerve. * **Chromatolysis:** The regenerative change seen in the **cell body** (soma) following axonal injury, characterized by swelling and displacement of the nucleus.
Question 10: Maximum conduction occurs in which type of nerve fibers?
- A. B fibers
- B. A alpha fibers (Correct Answer)
- C. Sympathetic fibers
- D. C fibers
Explanation: **Explanation:** The velocity of nerve impulse conduction is primarily determined by two factors: **fiber diameter** and the **presence of myelin**. According to the Erlanger-Gasser classification, nerve fibers are categorized based on these properties. **1. Why A alpha fibers are correct:** A alpha fibers are the **thickest** (12–20 µm) and most **heavily myelinated** nerve fibers in the body. According to the principles of cable theory, a larger diameter reduces internal resistance to current flow, while myelin provides saltatory conduction. This combination allows A alpha fibers to achieve the maximum conduction velocity (approximately **70–120 m/sec**). They primarily carry motor impulses to skeletal muscles and sensory information from proprioceptors (muscle spindles and Golgi tendon organs). **2. Why the other options are incorrect:** * **B fibers:** These are preganglionic autonomic fibers. While myelinated, they have a much smaller diameter ( <3 µm) than A fibers, resulting in slower conduction (3–15 m/sec). * **C fibers:** These are the slowest of all nerve fibers (0.5–2 m/sec) because they are **unmyelinated** and have the smallest diameter. They carry slow pain, temperature, and postganglionic autonomic impulses. * **Sympathetic fibers:** Most postganglionic sympathetic fibers are C fibers (unmyelinated), making them among the slowest conductors. **High-Yield Clinical Pearls for NEET-PG:** * **Order of Susceptibility:** * **Hypoxia:** B fibers are most sensitive (B > A > C). * **Pressure:** A fibers are most sensitive (A > B > C). * **Local Anesthetics:** C fibers are most sensitive (C > B > A). * **Fastest to Slowest:** Aα > Aβ > Aγ > Aδ > B > C. * **A delta (Aδ) fibers** carry "fast pain" (sharp/localized), while **C fibers** carry "slow pain" (dull/aching).
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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