Nerve and Muscle Physiology Practice Questions

Q: Tetany may be present in all the following conditions except?

Hyperkalemia. Tetany is a state of increased neuromuscular excitability characterized by carpopedal spasms, paresthesia, and laryngospasm. It is primarily caused by a decrease in the threshold for nerve depolarization. **Why Hyperkalemia is the Correct Answer:** Hyperkalemia (Option C) actually **decreases** neuromuscular excitability by causing persistent depolarization of the cell membrane, which eventually leads to a state of inactivation of sodium channels (refractoriness) [1]. This typically results in muscle weakness or paralysis, not tetany. In contrast, **Hypokalemia** can occasionally be associated with tetany, particularly when it coexists with metabolic alkalosis. **Analysis of Incorrect Options:** * **Acute Pancreatitis (Option A):** This condition often leads to **hypocalcemia** due to the saponification of calcium in necrotic fat (calcium soaps) [2]. Low ionized calcium levels reduce the threshold for action potentials, leading to tetany. * **Hysterical Hyperventilation (Option B):** Hyperventilation causes respiratory alkalosis. The increase in blood pH promotes the binding of ionized calcium to albumin, leading to **decreased ionized calcium** levels (despite normal total calcium), which triggers tetany [2]. * **Hypomagnesemia (Option D):** Magnesium is a cofactor for PTH secretion and action. Severe magnesium deficiency leads to secondary hypocalcemia and can also directly increase neuromuscular excitability, both of which cause tetany [2]. **NEET-PG High-Yield Pearls:** * **Trousseau’s Sign:** Induction of carpal spasm by inflating a BP cuff above systolic pressure for 3 minutes (more sensitive than Chvostek). * **Chvostek’s Sign:** Tapping the facial nerve leads to twitching of facial muscles. * **The "Ionized" Rule:** Tetany is always a function of **ionized calcium** levels, not total calcium [2]. * **Metabolic Alkalosis:** Always consider tetany in alkalotic states due to increased calcium-albumin binding [2].

Q: Following repolarization, a neuron may become hyperpolarized. How does the membrane potential subsequently return to the resting membrane potential (RMP)?

Inward leakage of Na+ ions. **Explanation:** The return of the membrane potential to the Resting Membrane Potential (RMP) after hyperpolarization is a passive process primarily driven by the **inward leakage of Na+ ions**. 1. **Why Option B is Correct:** During the undershoot (hyperpolarization), the membrane potential is closer to the equilibrium potential of K+ (-94 mV) than the RMP (-70 mV). At this stage, the membrane is highly permeable to K+ but also possesses **non-gated "leak" channels**. Because the electrochemical gradient for Na+ is very high (high concentration outside, negative charge inside), Na+ ions slowly leak into the cell. This influx of positive charge gradually depolarizes the membrane back to its steady-state RMP. 2. **Why Other Options are Incorrect:** * **Option A (Na+/K+-ATPase):** While this pump is essential for maintaining long-term concentration gradients, it is **electrogenic** (pumping 3 Na+ out for 2 K+ in). Its net effect is to make the interior *more* negative. Therefore, it helps maintain or establish RMP but is not the primary mechanism that "pulls" the potential up from a hyperpolarized state. * **Option C (Decrease in K+ efflux):** While the closing of voltage-gated K+ channels stops further hyperpolarization, it does not actively return the potential to RMP; it merely prevents it from getting more negative. **High-Yield NEET-PG Pearls:** * **RMP** is primarily determined by **K+ efflux** through leak channels (K+ permeability is 50–100x higher than Na+ at rest). * **Hyperpolarization** occurs because voltage-gated K+ channels are slow to close. * **The Goldmann-Hodgkin-Katz equation** is used to calculate RMP considering multiple ions, whereas the **Nernst equation** is for a single ion.

Q: End plate potential follows which law?

Depolarization. **Explanation:** The **End Plate Potential (EPP)** is a localized, non-propagated potential change that occurs at the motor end plate of the neuromuscular junction (NMJ). **1. Why Depolarization is Correct:** When an action potential reaches the motor nerve terminal, it triggers the release of Acetylcholine (ACh). ACh binds to nicotinic receptors (nAChR) on the motor end plate, opening ligand-gated cation channels. This leads to a massive influx of **Na⁺ ions** (and a smaller efflux of K⁺), causing the resting membrane potential to shift toward a more positive value. This process is, by definition, **Depolarization**. If the EPP reaches a certain threshold, it triggers a propagated action potential in the muscle fiber. **2. Why other options are incorrect:** * **All or none law:** Unlike an action potential, the EPP is a **graded potential**. Its magnitude depends on the amount of ACh released; it does not follow the all-or-none law. * **Hyperpolarization:** This involves the membrane potential becoming more negative. EPP is excitatory and always involves a shift toward positivity. * **Propagation:** EPP is a **local potential**. It does not travel down the muscle fiber; instead, it triggers an action potential which then propagates. **High-Yield Clinical Pearls for NEET-PG:** * **Miniature End Plate Potential (MEPP):** The smallest possible EPP caused by the spontaneous release of a single vesicle (quantum) of ACh. * **Myasthenia Gravis:** Antibodies against nAChR reduce the amplitude of the EPP, making it difficult to reach the threshold for muscle contraction. * **Lambert-Eaton Syndrome:** Antibodies against voltage-gated Ca²⁺ channels reduce ACh release, also resulting in a decreased EPP. * **Curare:** Competitively inhibits nAChR, decreasing the EPP amplitude and causing paralysis.

Q: Small nerve fibers carry all except:

Position sense. **Explanation:** The classification of nerve fibers is based on diameter and conduction velocity (Erlanger-Gasser classification). The core principle is that **fiber diameter is directly proportional to conduction velocity and the degree of myelination.** **1. Why "Position Sense" is the correct answer:** Position sense (proprioception) is carried by the largest, most heavily myelinated fibers in the body, specifically **Type Ia** (from muscle spindles) and **Type Ib** (from Golgi tendon organs) fibers, or **Type A-alpha** fibers. These fibers require rapid conduction velocities (70–120 m/s) to provide the brain with real-time feedback on body posture and movement. Therefore, they are the opposite of "small" fibers. **2. Why the other options are incorrect:** * **Pain and Cold (A & D):** These are primarily carried by **Type A-delta** fibers. These are small, thinly myelinated fibers that transmit "fast" pain and cold sensations. * **Heat and Slow Pain (B):** These are carried by **Type C** fibers. These are the smallest nerve fibers and are completely **unmyelinated**, resulting in slow conduction velocities (0.5–2 m/s). **High-Yield Clinical Pearls for NEET-PG:** * **Order of Susceptibility:** * **Local Anesthetics:** Block **Small** fibers first (Type C > B > A). Clinically, pain is lost before touch and pressure. * **Hypoxia:** Blocks **Large** fibers first (Type A > B > C). * **Pressure:** Blocks **Large** fibers first (Type A > B > C). This is why your limb "falls asleep" (loss of touch/motor) before you lose the ability to feel pain. * **Type B fibers** are preganglionic autonomic fibers and are the most sensitive to hypoxia. * **Type C fibers** are the only unmyelinated fibers and carry the majority of "slow/chronic" pain.

Q: Calmodulin acts by:

Phosphorylation of myosin by protein kinase. **Explanation:** **Mechanism of Action (Why Option B is correct):** Calmodulin is a calcium-binding messenger protein found in all eukaryotic cells. In smooth muscle contraction, it plays a pivotal role because smooth muscle lacks the troponin complex found in skeletal muscle. When intracellular $Ca^{2+}$ levels rise, four $Ca^{2+}$ ions bind to **Calmodulin**, forming a $Ca^{2+}$-Calmodulin complex. This complex activates an enzyme called **Myosin Light Chain Kinase (MLCK)**. MLCK then **phosphorylates** the regulatory light chain of the myosin head. This phosphorylation increases myosin ATPase activity, allowing the myosin head to bind to actin and initiate the cross-bridge cycle (contraction). **Why other options are incorrect:** * **Option A:** Sodium channel opening is typically mediated by voltage changes (action potentials) or ligand binding (e.g., Acetylcholine), not by Calmodulin. * **Option C:** The $Na^{+}$-$K^{+}$ pump is primarily regulated by ATP availability and specific hormones (like insulin or aldosterone), not directly by the Calmodulin-MLCK pathway. * **Option D:** Dephosphorylation of myosin leads to **relaxation**, not contraction. This process is mediated by **Myosin Light Chain Phosphatase (MLCP)**, which removes the phosphate group that MLCK added. **High-Yield Clinical Pearls for NEET-PG:** * **Stoichiometry:** 1 Calmodulin binds to **4 Calcium ions**. * **Smooth Muscle Relaxation:** Nitric Oxide (NO) causes relaxation by increasing cGMP, which inhibits MLCK and activates MLCP. * **Troponin vs. Calmodulin:** Remember the mnemonic: **S**keletal muscle uses **S**troke/Troponin; **S**mooth muscle uses **S**econd messenger/Calmodulin. * **Other functions:** Calmodulin also regulates the activation of phosphorylase kinase in glycogenolysis and modulates cyclic nucleotide phosphodiesterase.

Q: What is true about generator potential?

Graded. ### Explanation **Generator Potential** (also known as Receptor Potential) is the non-propagated local electrical response produced in a sensory receptor by a stimulus. **1. Why "Graded" is Correct:** Generator potentials are **graded**, meaning the amplitude of the potential is directly proportional to the intensity of the stimulus. Unlike action potentials, which have a fixed amplitude, a stronger stimulus results in a larger generator potential. Once this potential reaches a specific threshold, it triggers an action potential in the sensory nerve fiber. **2. Why the Other Options are Incorrect:** * **B. All or none:** This law applies to **Action Potentials**, not generator potentials. Generator potentials do not have a threshold for initiation and can vary in size. * **C. Propagated:** Generator potentials are **non-propagated** (local) responses. They spread passively via electrotonic conduction and decay over distance. Only action potentials are propagated along the axon. * **D. No summation:** Generator potentials **can be summated** (both temporally and spatially). If multiple stimuli are applied, the potentials add up to reach the threshold required to fire an action potential. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Usually involves the opening of non-specific cation channels (Na+ influx). * **Refractory Period:** Generator potentials have **no refractory period**, allowing for the summation of signals. * **Example:** The **Pacinian Corpuscle** is the classic model used to study generator potentials. If the first node of Ranvier is blocked (e.g., by local anesthetics), the generator potential still occurs, but the action potential is abolished. * **Key Distinction:** Generator potential = Graded, Local, Summable; Action potential = All-or-none, Propagated, Refractory period present.

Question 1

Which of the following statements is FALSE regarding the stretch reflex?

Accepted Answer

Relaxation of the muscle is the response.

Answer

Stretch of the muscle initiates the reflex.

Answer

The muscle spindle is the sense organ.

Answer

Impulses are conducted by fast sensory fibers.

Question 2

If a supramaximal stimulus is applied to an excitable tissue like a nerve or a muscle and it elicits a response, then the tissue is said to be in which state?

Accepted Answer

Relative refractory period

Answer

Absolute refractory period

Answer

Latent period

Answer

After-depolarization

Question 3

Tetany may be present in all the following conditions except?

Accepted Answer

Hyperkalemia

Answer

Acute pancreatitis

Answer

Hysterical hyperventilation

Answer

Hypomagnesemia

Question 4

Following repolarization, a neuron may become hyperpolarized. How does the membrane potential subsequently return to the resting membrane potential (RMP)?

Accepted Answer

Inward leakage of Na+ ions

Answer

Action of the Na+/K+-ATPase pump

Answer

Decrease in K+ ion efflux

Answer

None of the above mechanisms

Question 5

End plate potential follows which law?

Accepted Answer

Depolarization

Answer

All or none law

Answer

Hyperpolarization

Answer

Propagation

Question 6

Small nerve fibers carry all except:

Accepted Answer

Position sense

Answer

Cold

Answer

Heat

Answer

Pain

Question 7

Calmodulin acts by:

Accepted Answer

Phosphorylation of myosin by protein kinase

Answer

Opening of Na+ channels

Answer

Activation of the Na+-K+ pump

Answer

Dephosphorylation by protein kinase

Question 8

What is true about generator potential?

Accepted Answer

Graded

Answer

All or none

Answer

Propagated

Answer

No summation

Question 9

What type of cell junction is found in smooth muscle?

Accepted Answer

Gap junction

Answer

Zonula adherens

Answer

Macula adherens

Answer

Tight junction

Question 10

Which of the following muscle groups exhibits isometric contraction?

Accepted Answer

Antigravity muscles

Answer

Extraocular muscles

Answer

Small muscles of the hand

Answer

Abdominal muscles

Nerve and Muscle Physiology — MCQs

Nerve and Muscle Physiology — MCQs

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