When the nurse administers a drug that stimulates the nicotinic receptors, what manifestation would indicate that the drug is working?

A) Pupil constriction: Pupil constriction (miosis) is primarily mediated by the parasympathetic nervous system through muscarinic receptors, not nicotinic receptors. Nicotinic receptors, when stimulated, affect skeletal muscle contraction, not the size of the pupils.

B) Muscle contraction: Nicotinic receptors are located on skeletal muscle cells and are responsible for mediating muscle contraction when activated. When a drug stimulates nicotinic receptors, the expected outcome is muscle contraction, as these receptors play a critical role in neuromuscular transmission.

C) Increase GI motility: While nicotinic receptors are involved in muscle contraction, they are not the primary mediators of gastrointestinal motility. Muscarinic receptors, which are part of the parasympathetic nervous system, primarily control GI motility. Stimulating muscarinic receptors would lead to increased motility, but not nicotinic receptors.

D) Decrease in heart rate: A decrease in heart rate is typically associated with the stimulation of muscarinic receptors, particularly those that influence the parasympathetic nervous system (vagal tone). Nicotinic receptor activation does not directly influence heart rate; in fact, their stimulation is more related to skeletal muscle contraction.

A) Excessive salivation: Neostigmine (Prostigmin) is a cholinesterase inhibitor, which works by increasing the levels of acetylcholine at neuromuscular junctions. If a dose is missed, excessive salivation can be a side effect of too much acetylcholine activity, but it is not the most immediate symptom in this case. Muscle weakness is a more direct consequence of a missed dose.

B) Respiratory paralysis: While respiratory weakness or paralysis can occur in myasthenia gravis, it is usually associated with a severe form of the disease or if the patient is in a myasthenic crisis. A single missed dose of neostigmine typically does not result in respiratory failure unless the patient is already in a very fragile state.

C) Muscle weakness: Neostigmine helps to improve neuromuscular transmission by inhibiting the breakdown of acetylcholine, which is crucial for muscle contraction. A missed dose would directly lead to a reduction in acetylcholine levels, exacerbating the characteristic muscle weakness of myasthenia gravis. Muscle weakness is the most anticipated symptom when neostigmine is not administered on time.

D) Muscle spasms: Muscle spasms are typically not a symptom of missed neostigmine therapy. Instead, muscle weakness occurs due to impaired neuromuscular transmission. Spasms might occur if there is significant overstimulation of the muscles, but this is more associated with electrolyte imbalances or other neuromuscular issues