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Here are detailed answers to all visible questions (15-22), with the correct answers marked and explained:

Questions 15-22: Neuroscience/Physiology MCQs

Q15. Antibodies against voltage-gated calcium channels in the nerve terminal

Correct Answer: c. Lambert-Eaton syndrome

Lambert-Eaton myasthenic syndrome is an autoimmune disorder where antibodies target presynaptic P/Q-type voltage-gated calcium channels (VGCCs) at the neuromuscular junction. This impairs calcium influx needed to trigger acetylcholine vesicle exocytosis, causing proximal muscle weakness. It is frequently associated with small cell lung carcinoma. - Adams and Victor's Principles of Neurology and Miller's Anesthesia

Myasthenia gravis (b) involves antibodies against postsynaptic ACh receptors, not calcium channels.
Duchenne (a) is a genetic dystrophin mutation; MS (d) is CNS demyelination; Tetanus (e) is due to tetanospasmin toxin.

Q16. Ion movement most responsible for IPSP

Correct Answer: e. Chloride efflux -- Wait, let me be precise here.

The correct answer is actually c. Potassium efflux OR more classically, chloride influx (not efflux). Looking at the options carefully:

The options are: a) Sodium influx, b) Calcium influx, c) Potassium efflux, d) Potassium influx, e) Chloride efflux.

Per Guyton and Hall and Katzung: IPSPs are produced by opening of chloride channels (chloride influx, not efflux) AND potassium efflux channels. The chloride ions flow into the cell (influx), hyperpolarizing it. Potassium efflux also causes hyperpolarization.

Since "chloride influx" is not among the options but "chloride efflux" is listed as option (e), and the image shows option (e) is circled/crossed, the best answer from the given options is c. Potassium efflux, which correctly hyperpolarizes the membrane by moving positive charge out. Chloride efflux would actually depolarize, so that option is a distractor.

Correct Answer: c. Potassium efflux - K+ leaving the cell causes hyperpolarization = IPSP. - Guyton and Hall, Ganong's Review

Q17. Synapsin proteins defective - no ACh vesicle fusion

Correct Answer: b. Failure of neuromuscular transmission

Synapsins are proteins that anchor synaptic vesicles to the cytoskeleton. When defective, vesicles cannot dock and fuse with the presynaptic membrane, so ACh is not released into the synaptic cleft. Without ACh binding to postsynaptic nicotinic receptors, no end-plate potential (EPP) is generated and neuromuscular transmission fails entirely. There is no depolarization, no muscle contraction.

Q18. Peripheral nerve crushed - distal segment degenerates

Correct Answer: c. Wallerian degeneration

When a peripheral axon is severed or crushed, the segment distal to the injury (cut off from the cell body) undergoes Wallerian degeneration - the axon and its myelin sheath break down and are cleared by Schwann cells and macrophages. This begins within 24-48 hours and progresses over days to weeks. - Miller's Review of Orthopaedics

Chromatolysis (a) is the reaction in the cell body (retrograde change), not the distal segment.
Saltatory conduction (b) is normal nerve impulse propagation.

Q19. Severe hypokalemia - change in nerve fibers

Correct Answer: c. Hyperpolarization

In hypokalemia, extracellular K+ is low. The equilibrium potential for K+ (EK) becomes more negative (more hyperpolarized), because the outward K+ gradient increases. As EK drives the resting membrane potential, the cell hyperpolarizes - moving the membrane further from threshold. This paradoxically makes the nerve less excitable (hyperpolarization). In severe hypokalemia, this can cause muscle weakness and even paralysis.

Mnemonic: Low extracellular K+ → bigger K+ gradient → more K+ leaves → more negative inside = hyperpolarization.

Q20. Local anesthetic blocks voltage-gated Na+ channels - phase prevented

Correct Answer: c. Depolarization

Local anesthetics (e.g., lidocaine) bind to and block voltage-gated sodium channels, preventing the rapid Na+ influx that causes the rising phase of the action potential - which is depolarization. As Rosen's Emergency Medicine and Roberts and Hedges confirm: "Local anesthetic agents reversibly block lipid membrane sodium channels and prevent the influx of sodium ions into the axon, blocking depolarization and the nerve action potential."

Q21. Stimulation during absolute refractory period - second AP fails because:

Correct Answer: b. Sodium channels remain inactivated

During the absolute refractory period, voltage-gated Na+ channels are in their inactivated state (the inactivation gate is closed). They cannot be reopened by any stimulus, no matter how strong, until they reset to the closed/resting state. This is why no second action potential can be generated. - Guyton and Hall

Q22. Sympathetic nerves destroyed - organ becomes supersensitive to norepinephrine

Correct Answer: Denervation supersensitivity (the phenomenon is called denervation hypersensitivity/supersensitivity)

When sympathetic nerves are destroyed, the denervated smooth muscle upregulates its adrenergic receptors (receptor upregulation) and loses neuronal reuptake of norepinephrine (since no nerve terminals remain). The organ becomes excessively responsive to exogenous norepinephrine. This is called denervation supersensitivity (or Cannon's law of denervation). - Katzung's Basic and Clinical Pharmacology

Summary Table

Q	Correct Answer	Key Concept
15	c. Lambert-Eaton syndrome	Anti-presynaptic VGCC antibodies
16	c. Potassium efflux	K+ efflux hyperpolarizes → IPSP
17	b. Failure of NMJ transmission	Synapsins needed for vesicle docking/fusion
18	c. Wallerian degeneration	Distal axon breakdown after nerve crush
19	c. Hyperpolarization	Low extracellular K+ → more negative RMP
20	c. Depolarization	LA blocks Na+ influx = no depolarization
21	b. Na+ channels remain inactivated	Absolute refractory period mechanism
22	Denervation supersensitivity	Receptor upregulation after nerve loss

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