Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology Indian Medical PG Practice Questions and MCQs

Question 351: Which of the following mechanisms actively maintains the ionic concentration gradients essential for the resting membrane potential in neurons?

A. Sodium-potassium pump (Correct Answer)
B. Calcium channels
C. Chloride channels
D. Voltage-gated sodium channels

Explanation: ***Sodium-potassium pump*** - The **sodium-potassium pump (Na⁺/K⁺-ATPase)** actively transports **3 sodium ions out** and **2 potassium ions into** the cell, requiring ATP. - This establishes and maintains the **concentration gradients** (high K⁺ inside, high Na⁺ outside) that are essential for the resting membrane potential. - While **potassium leak channels** create the primary electrical potential (~-70 mV), the pump maintains the gradients that allow these channels to function and contributes an additional **-5 to -10 mV** through its electrogenic activity. *Calcium channels* - **Calcium channels** mediate **calcium influx** during action potentials, triggering neurotransmitter release and other cellular processes. - They do not establish or maintain the ionic gradients responsible for the **resting membrane potential**. *Chloride channels* - **Chloride channels** help stabilize membrane potential and mediate inhibitory signals but do not actively maintain the primary **Na⁺ and K⁺ gradients** underlying resting potential. - They play a secondary role compared to the active transport mechanisms. *Voltage-gated sodium channels* - **Voltage-gated sodium channels** are closed at rest and open during **action potential depolarization** to allow rapid Na⁺ influx. - They propagate action potentials but do not maintain the resting concentration gradients.

Question 352: A patient experiences sudden muscle weakness after consuming a large amount of potassium-rich food. Which physiological mechanism is likely responsible for the muscle weakness?

A. Decreased potassium efflux
B. Increased sodium influx
C. Depolarization of the nerve membrane (Correct Answer)
D. Hyperpolarization of the nerve membrane

Explanation: ***Depolarization of the nerve membrane*** - A large intake of potassium-rich food can lead to **hyperkalemia**, causing the **resting membrane potential** of nerve and muscle cells to become less negative (depolarized). - While initial depolarization can fire action potentials, sustained depolarization inactivates **voltage-gated sodium channels**, preventing further firing and leading to **muscle weakness** or paralysis. *Decreased potassium efflux* - In situations of hyperkalemia, there might be a *relative* decrease in potassium efflux compared to the elevated extracellular potassium, but the primary mechanism leading to weakness is due to the sustained depolarization of the membrane. - Reduced potassium efflux wouldn't directly cause muscle weakness; rather, it would contribute to the inability to repolarize effectively. *Increased sodium influx* - While depolarization is linked to sodium channel function, the underlying issue in hyperkalemia leading to weakness is the sustained depolarization that inactivates these channels, not an increased sodium influx itself. - An uncontrolled increase in sodium influx would typically lead to increased excitability, not weakness, unless it's part of a cycle that inactivates voltage-gated channels. *Hyperpolarization of the nerve membrane* - **Hyperpolarization** would make the nerve membrane more negative and *less* excitable, eventually leading to muscle weakness by making it harder to reach the threshold for an action potential. - However, **hyperkalemia** causes **depolarization** (less negative resting membrane potential), making this option incorrect for the given scenario.

Question 353: Which ion primarily determines the resting membrane potential of excitable cells?

A. Sodium
B. Chloride
C. Calcium
D. Potassium (Correct Answer)

Explanation: ***Potassium*** - The resting membrane potential is primarily determined by the **efflux of potassium ions** through **leak channels**, making the inside of the cell more negative. - The high **intracellular concentration of potassium** and the greater permeability of the membrane to potassium at rest are key factors. *Sodium* - While sodium channels are critical for the **depolarization phase** of an action potential, the cell membrane is much less permeable to **sodium** at rest. - The **sodium-potassium pump** actively transports sodium out of the cell, contributing indirectly to the resting potential. *Chloride* - **Chloride ions** can influence the resting membrane potential, particularly in certain cells, but their contribution is generally less significant than potassium. - In many neurons, chloride flow helps to **stabilize or hyperpolarize** the membrane, but it's not the primary determinant of the resting state. *Calcium* - **Calcium ions** are crucial for various cellular processes, including neurotransmitter release and muscle contraction, but they play a minimal direct role in establishing the resting membrane potential. - The cell maintains a very **low intracellular calcium concentration**, and its channels are largely closed at rest.

Question 354: A patient presents with symptoms of muscle weakness and fatigue. Serum potassium levels are significantly elevated. How does hyperkalemia affect the resting membrane potential and action potential generation in neurons?

A. Hyperpolarizes the resting membrane potential, making action potentials harder to generate
B. No change in resting membrane potential, no change in action potential generation
C. Hyperpolarizes the resting membrane potential, making action potentials easier to generate
D. Depolarizes the resting membrane potential, making action potentials harder to generate (Correct Answer)

Explanation: ***Depolarizes the resting membrane potential, making action potentials harder to generate*** - Hyperkalemia causes the **extracellular potassium concentration** to rise, which leads to a **less negative resting membrane potential** (depolarization), bringing it closer to the threshold for action potential firing. - However, prolonged depolarization **inactivates voltage-gated sodium channels**, making them unresponsive to further stimulation and **preventing the generation of new action potentials**. - This explains the **paradoxical muscle weakness** seen in hyperkalemia despite initial membrane depolarization. *Hyperpolarizes the resting membrane potential, making action potentials harder to generate* - This statement incorrectly suggests that hyperkalemia causes hyperpolarization (more negative resting potential). Hyperkalemia actually **depolarizes** (makes less negative) the resting membrane potential. - While hyperpolarization would make action potentials harder to generate, this is not the mechanism in hyperkalemia. *Hyperpolarizes the resting membrane potential, making action potentials easier to generate* - This is incorrect because hyperkalemia causes **depolarization**, not hyperpolarization of the resting membrane potential. - Hyperpolarization would move the membrane potential further from threshold, making action potentials harder, not easier to generate. *No change in resting membrane potential, no change in action potential generation* - This is incorrect as serum potassium levels are a primary determinant of the **resting membrane potential** of excitable cells according to the **Nernst equation**. - Significant changes in potassium levels directly alter the **electrochemical gradient** and the membrane potential, thereby affecting excitability.

Question 355: A neurology patient exhibits muscle weakness and fatigue. Electromyography shows a decreased amplitude of muscle action potentials. Which ion channel malfunction is most likely responsible for this finding?

A. Calcium channels in the sarcoplasmic reticulum
B. Sodium channels in the sarcolemma (Correct Answer)
C. Potassium channels in the sarcolemma
D. Chloride channels in the sarcolemma

Explanation: ***Sodium channels in the sarcolemma*** - A **decreased amplitude of muscle action potentials** indicates a problem with the generation or propagation of electrical signals in the muscle membrane. - **Voltage-gated sodium channels** in the sarcolemma are primarily responsible for the **rapid depolarization and amplitude** of muscle action potentials. - Malfunction of these channels, such as in **sodium channelopathies** (e.g., hyperkalemic periodic paralysis, paramyotonia congenita), can lead to insufficient depolarization and reduced action potential amplitude, resulting in muscle weakness. - The amplitude of the action potential is directly determined by the magnitude of **sodium influx** during the depolarization phase. *Calcium channels in the sarcoplasmic reticulum* - These channels are crucial for **calcium release** from the sarcoplasmic reticulum into the cytoplasm, initiating the contractile process through **excitation-contraction coupling**. - While essential for muscle contraction strength, their malfunction would not directly affect the **amplitude of the sarcolemmal action potential** recorded on EMG, which reflects electrical activity of the muscle membrane. *Potassium channels in the sarcolemma* - **Potassium channels** are mainly responsible for **repolarization** of the muscle fiber and maintaining the resting membrane potential. - Their malfunction can affect muscle excitability and may cause prolonged depolarization (as in some periodic paralyses), but they do not primarily determine the **amplitude** of the action potential, which depends on sodium influx during the upstroke. *Chloride channels in the sarcolemma* - **Chloride channels** play a significant role in **stabilizing the resting membrane potential** and regulating muscle excitability. - Dysfunction in chloride channels typically leads to conditions like **myotonia congenita** (delayed muscle relaxation and hyperexcitability), but not to decreased amplitude of muscle action potentials or the pattern of weakness and fatigue described.

Question 356: Which of the following best describes the role of the sarcoplasmic reticulum in muscle cells?

A. Stores calcium ions (Correct Answer)
B. Generates ATP
C. Contains actin and myosin
D. Produces muscle proteins

Explanation: ***Stores calcium ions*** - The **sarcoplasmic reticulum (SR)** is a specialized endoplasmic reticulum in muscle cells that primarily functions as a **storage site for Ca2+ ions**. - During muscle contraction, the SR releases stored **calcium ions** into the sarcoplasm, which then bind to troponin, initiating the contractile process. *Generates ATP* - The primary organelle responsible for **ATP generation** in muscle cells is the **mitochondria**, through cellular respiration. - While muscle contraction requires ATP, the **sarcoplasmic reticulum** itself does not produce it. *Contains actin and myosin* - **Actin and myosin** are the primary contractile proteins found within the **myofibrils** of muscle cells, not within the sarcoplasmic reticulum. - The sarcoplasmic reticulum surrounds the myofibrils but does not contain these filaments internally. *Produces muscle proteins* - **Muscle proteins** like actin and myosin are synthesized on **ribosomes** located in the cytoplasm or on the rough endoplasmic reticulum. - The **sarcoplasmic reticulum** is mainly involved in calcium handling, not protein synthesis.

Question 357: A patient with hypocalcemia presents with tetany. Which physiological process is most likely responsible for the muscle spasms?

A. Increased neuronal excitability (Correct Answer)
B. Decreased neuronal excitability
C. Increased muscle contractility
D. Decreased muscle contractility

Explanation: ***Increased neuronal excitability*** - **Hypocalcemia** reduces the extracellular calcium concentration, which destabilizes the neuronal membrane by reducing calcium's normal stabilizing effect on **voltage-gated sodium channels**. - This lowers the threshold for depolarization, making neurons **more excitable** and prone to spontaneous action potentials, resulting in the involuntary muscle contractions characteristic of **tetany**. - The mechanism: Ca²⁺ normally binds to negatively charged membrane sites, raising the voltage threshold needed for sodium channel activation. Low calcium removes this stabilization. *Decreased neuronal excitability* - This would lead to a reduction in nerve impulses and muscle activity, which is the opposite of what is seen in tetany. - Conditions causing decreased neuronal excitability often result in muscle weakness or paralysis, not spasms. *Increased muscle contractility* - While tetany involves muscle contraction, the primary issue in hypocalcemia is enhanced *neuronal* firing that *initiates* the contractions, not an inherent increase in the muscle's ability to contract independently of neuronal input. - Calcium's direct role in muscle contraction (binding to troponin) is largely intracellular and not the primary driver of tetany caused by *extracellular* hypocalcemia. *Decreased muscle contractility* - This would result in weaker muscle contractions or paralysis, which is contrary to the clinical presentation of tetany. - Decreased muscle contractility is not associated with hypocalcemia-induced spasms.

Question 358: A patient with severe muscle weakness is found to have reduced acetylcholine release at the neuromuscular junction. Which physiological process is most likely impaired?

A. Exocytosis of acetylcholine (Correct Answer)
B. Synthesis of acetylcholine
C. Reuptake of choline
D. Storage of acetylcholine in vesicles

Explanation: ***Exocytosis of acetylcholine*** - **Reduced acetylcholine release** directly indicates a problem with the process by which neurotransmitters are expelled from the presynaptic terminal, which is **exocytosis**. - Impaired exocytosis would lead to an insufficient amount of acetylcholine reaching the postsynaptic membrane, causing **severe muscle weakness**. - This is the most direct physiological explanation when the primary finding is **reduced release** at the neuromuscular junction. *Synthesis of acetylcholine* - While impaired synthesis would eventually lead to reduced release, the immediate problem described is **reduced release**, implying acetylcholine is present but not being liberated effectively. - Problems with synthesis often manifest as a more chronic, rather than acute, decline in neurotransmitter levels. - Synthesis occurs in the cytoplasm before vesicular packaging, so this is upstream from the release mechanism. *Reuptake of choline* - Impaired reuptake of choline would affect the *recycling* of choline for subsequent acetylcholine synthesis, but it does not directly explain an immediate reduction in the *release* of already synthesized acetylcholine. - This would primarily affect the long-term availability of neurotransmitter precursors, not the exocytotic process itself. - Choline reuptake occurs at the presynaptic terminal after ACh breakdown in the synaptic cleft. *Storage of acetylcholine in vesicles* - If storage were impaired, acetylcholine might be degraded within the presynaptic terminal rather than being packaged into vesicles for release. - This could lead to reduced release, but the question specifically points to the **release mechanism** as the primary issue. - When release is specifically impaired, the exocytotic machinery (calcium-dependent fusion and SNARE proteins) is most directly implicated.

Question 359: Which neurotransmitter primarily mediates the effects of the parasympathetic nervous system?

A. Dopamine
B. Norepinephrine
C. Acetylcholine (Correct Answer)
D. GABA

Explanation: ***Acetylcholine*** - **Acetylcholine** (ACh) is the primary neurotransmitter released by postganglionic neurons in the **parasympathetic nervous system**, mediating its "rest and digest" effects. - ACh acts on **muscarinic receptors** in target organs, leading to responses such as decreased heart rate, increased digestion, and pupillary constriction. *Dopamine* - **Dopamine** is primarily involved in reward, motivation, and motor control within the central nervous system, and it is not a primary mediator of the parasympathetic system. - While dopamine receptors exist in the peripheral nervous system, its role in mediating direct parasympathetic effects is limited compared to ACh. *Norepinephrine* - **Norepinephrine** is the primary neurotransmitter of the **sympathetic nervous system**, responsible for "fight or flight" responses. - It acts on **adrenergic receptors** at target organs, producing effects opposite to those of the parasympathetic system (e.g., increased heart rate, vasoconstriction). *GABA* - **GABA** (gamma-aminobutyric acid) is the main **inhibitory neurotransmitter** in the central nervous system, promoting relaxation and reducing neuronal excitability. - It has a negligible or indirect role in mediating the direct effector functions of the peripheral autonomic nervous system, particularly the parasympathetic branch.

Question 360: A patient presents with muscle cramps and tetany. Laboratory results show hypocalcemia. Which of the following physiological mechanisms is most likely responsible for these symptoms?

A. Increased binding of calcium to albumin
B. Decreased release of parathyroid hormone
C. Decreased neuronal excitability
D. Increased permeability to sodium (Correct Answer)

Explanation: ***Increased permeability to sodium*** - **Hypocalcemia** reduces the threshold for excitation, making nerve and muscle cells **hyperexcitable**. - This occurs because fewer calcium ions stabilize the cell membrane, leading to an easier influx of **sodium ions** and subsequent depolarization. *Decreased neuronal excitability* - This is incorrect as **hypocalcemia** actually leads to **increased neuronal excitability**, causing symptoms like tetany and cramps. - Reduced extracellular calcium increases membrane permeability to sodium, making it easier for neurons to fire action potentials. *Increased binding of calcium to albumin* - While increased binding of calcium to albumin (e.g., in alkalosis) can lead to **hypocalcemia**, it describes a cause of hypocalcemia, not the physiological mechanism directly responsible for the symptoms of muscle cramps and tetany. - The direct mechanism causing symptoms relates to the *effect* of reduced free calcium on nerve and muscle cell membranes. *Decreased release of parathyroid hormone* - **Decreased PTH release** is a common *cause* of hypocalcemia (e.g., hypoparathyroidism), but it is not the direct physiological mechanism behind the muscle cramps and tetany. - PTH regulates calcium levels but does not directly mediate the effect of low calcium on nerve and muscle cells.

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

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free